トップ›研究者一覧›橋本登

研究者を探す

研究者にアプローチする
更新情報を通知する

橋本登

徳島大学

プロフィール
教育活動
研究活動
社会活動
リサーチマップ・
Jグローバル
KAKEN
注目研究

研究者総覧で最新データを確認する

2024年5月17日更新

職名: 助教
電話: 研究者総覧に該当データはありませんでした。
電子メール: 研究者総覧に該当データはありませんでした。
学歴: 研究者総覧に該当データはありませんでした。
学位: 博士(医学) (名古屋大学) (2012年11月)
職歴・経歴: 2017/4: 徳島大学助教, 大学院医歯薬学研究部

専門分野・研究分野: 糖鎖生物学 (Glycobiology)

研究者総覧で最新データを確認する

2024年5月17日更新

専門分野・研究分野: 糖鎖生物学 (Glycobiology)
担当経験のある授業科目: 全身組織学 (学部)
全身組織学実習 (学部)
口腔組織学実習 (学部)
歯の解剖学 (学部)
歯の解剖学実習 (学部)
指導経験: 2人 (博士)

研究者総覧で最新データを確認する

2024年5月17日更新

専門分野・研究分野: 糖鎖生物学 (Glycobiology)

研究テーマ: 可溶性Siglec-9の抗炎症・組織再生効果の解明 (再生医療, 免疫 (immunity), Siglec)

著書

Furukawa Koichi, Ohmi Yuhsuke, Ohkawa Yuki, Noboru Hashimoto, Yamauchi Yoshio, Yajima Orie and Furukawa Keiko :
Gangliosides: Synthesis and function in nervous tissues,
Springer Japan, Jan. 2015. 古川鋼一, 大川祐樹, 橋本登, 大海雄介, 古川圭子 :
がん関連抗原としてのガングリオシド,
株式会社羊土社, 2013年6月.

論文

Linze Xia, Fumiya Kano, Noboru Hashimoto, Yao Liu, Tsendsuren Khurel-Ochir, Naoko Ogasawara, Cheng Ding, Yang Xu, Hideharu Hibi, Tomonori Iwasaki, Eiji Tanaka and Akihito Yamamoto :
Conditioned Medium From Stem Cells of Human Exfoliated Deciduous Teeth Alleviates Mouse Osteoarthritis by Inducing sFRP1-Expressing M2 Macrophages.,
Stem Cells Translational Medicine, Vol.13, No.4, 399-413, 2024.

(要約): Intravenous administration of conditioned medium from stem cells of human exfoliated deciduous teeth (SHED-CM) regenerates mechanically injured osteochondral tissues in mouse temporomandibular joint osteoarthritis (TMJOA). However, the underlying therapeutic mechanisms remain unclear. Here, we showed that SHED-CM alleviated injured TMJ by inducing anti-inflammatory M2 macrophages in the synovium. Depletion of M2 by Mannosylated Clodrosome abolished the osteochondral repair activities of SHED-CM. Administration of CM from M2-induced by SHED-CM (M2-CM) effectively ameliorated mouse TMJOA by inhibiting chondrocyte inflammation and matrix degradation while enhancing chondrocyte proliferation and matrix formation. Notably, in vitro, M2-CM directly suppressed the catabolic activities while enhancing the anabolic activities of interleukin-1β-stimulated mouse primary chondrocytes. M2-CM also inhibited receptor activator of nuclear factor NF-κB ligand-induced osteoclastogenesis in RAW264.7 cells. Secretome analysis of M2-CM and M0-CM revealed that 5 proteins related to anti-inflammation and/or osteochondrogenesis were enriched in M2-CM. Of these proteins, the Wnt signal antagonist, secreted frizzled-related protein 1 (sFRP1), was the most abundant and played an essential role in the shift to anabolic chondrocytes, suggesting that M2 ameliorated TMJOA partly through sFRP1. This study suggests that secretome from SHED exerted remarkable osteochondral regeneration activities in TMJOA through the induction of sFRP1-expressing tissue-repair M2 macrophages.
(キーワード): Humans / Mice / Animals / Culture Media, Conditioned / Stem Cells / Macrophages / Osteoarthritis / Anti-Inflammatory Agents / Tooth, Deciduous
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/stcltm/szae006
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38366885; ● Summary page in Scopus @ Elsevier: 2-s2.0-85190754023

(DOI: 10.1093/stcltm/szae006, PubMed: 38366885, Elsevier: Scopus) Linze XIA, Fumiya Kano, Noboru Hashimoto, Cheng DING, Yang XU, Hideharu HIBI, Tomonori Iwasaki, Eiji Tanaka and Akihito Yamamoto :
Conditioned Medium from Stem Cells of Human Exfoliated Deciduous Teeth Partially Alters the Expression of Inflammation-associated Molecules of Mouse Condylar Chondrocytes via Secreted Frizzled-related Protein 1,
Journal of Oral Health and Biosciences, Vol.35, No.2, 52-60, 2023.

(徳島大学機関リポジトリ): ● Metadata: 118150
(出版サイトへのリンク): ● Publication site (DOI): 10.20738/johb.35.2_52
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.20738/johb.35.2_52

(徳島大学機関リポジトリ: 118150, DOI: 10.20738/johb.35.2_52) Fumiya Kano, Noboru Hashimoto, Yao Liu, Linze Xia, Takaaki Nishihara, Wakana Oki, Keita Kawarabayashi, Noriko Mizusawa, Keiko Aota, Takayoshi Sakai, Masayuki Azuma, Hideharu Hibi, Tomonori Iwasaki, Tsutomu Iwamoto, Nobuyasu Horimai and Akihito Yamamoto :
Therapeutic benefits of factors derived from stem cells from human exfoliated deciduous teeth for radiation-induced mouse xerostomia,
Scientific Reports, Vol.13, No.1, 2706-2719, 2023.

(要約): Radiation therapy for head and neck cancers is frequently associated with adverse effects on the surrounding normal tissue. Irreversible damage to radiation-sensitive acinar cells in the salivary gland (SG) causes severe radiation-induced xerostomia (RIX). Currently, there are no effective drugs for treating RIX. We investigated the efficacy of treatment with conditioned medium derived from stem cells from human exfoliated deciduous teeth (SHED-CM) in a mouse RIX model. Intravenous administration of SHED-CM, but not fibroblast-CM (Fibro-CM), prevented radiation-induced cutaneous ulcer formation (p < 0.0001) and maintained SG function (p < 0.0001). SHED-CM treatment enhanced the expression of multiple antioxidant genes in mouse RIX and human acinar cells and strongly suppressed radiation-induced oxidative stress. The therapeutic effects of SHED-CM were abolished by the superoxide dismutase inhibitor diethyldithiocarbamate (p < 0.0001). Notably, quantitative liquid chromatography-tandem mass spectrometry shotgun proteomics of SHED-CM and Fibro-CM identified eight proteins activating the endogenous antioxidant system, which were more abundant in SHED-CM than in Fibro-CM (p < 0.0001). Neutralizing antibodies against those activators reduced antioxidant activity of SHED-CM (anti-PDGF-D; p = 0.0001, anti-HGF; p = 0.003). Our results suggest that SHED-CM may provide substantial therapeutic benefits for RIX primarily through the activation of multiple antioxidant enzyme genes in the target tissue.
(キーワード): Mice / Humans / Animals / Antioxidants / Stem Cells / Disease Models, Animal / Xerostomia / Tooth, Deciduous
(徳島大学機関リポジトリ): ● Metadata: 118051
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41598-023-29176-w
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36792628; ● Summary page in Scopus @ Elsevier: 2-s2.0-85148115146

(徳島大学機関リポジトリ: 118051, DOI: 10.1038/s41598-023-29176-w, PubMed: 36792628, Elsevier: Scopus) YAO LIU, Fumiya Kano, Noboru Hashimoto, LINZE XIA, Qiao Zhou, Xingmei Feng, Hideharu Hibi, Aya Miyazaki, Tsutomu Iwamoto, Yoshizo Matsuka, Zhijun Zhang, Eiji Tanaka and Akihito Yamamoto :
Conditioned Medium From the Stem Cells of Human Exfoliated Deciduous Teeth Ameliorates Neuropathic Pain in a Partial Sciatic Nerve Ligation Model.,
Frontiers in Pharmacology, Vol.13, 745020, 2022.

(要約): In neuropathic pain (NP), injury or diseases of the somatosensory system often result in highly debilitating chronic pain. Currently, there is no effective drug for the complete and definitive treatment of NP. We investigated the therapeutic potential of conditioned medium (CM) derived from stem cells from human exfoliated deciduous teeth (SHED-CM) against NP using a mouse partial sciatic nerve ligation (PSL) model. Abnormal pain sensation, such as tactile allodynia and hyperalgesia, can be caused by PSL. In the behavioral test, intravenous administration of SHED-CM greatly improved the PSL-induced hypersensitivity. We found that treatment with SHED-CM resulted in the recruitment of M2 macrophages in the injured sciatic nerve and ipsilateral L4/L5 dorsal root ganglion and suppressed microglial activation in the spinal cord. Notably, specific depletion of the anti-inflammatory M2 macrophages by mannosylated-Clodrosome markedly reduced the antinociceptive effect of SHED-CM. Intravenous administration of CM from M2 induced by SHED-CM (M2-CM) ameliorated the PSL-induced hypersensitivity. We found that M2-CM directly suppressed the expression of nociceptive receptors as well as proinflammatory mediators in Schwann cells. Taken together, our data suggest that SHED-CM ameliorates NP through the induction of the analgesic anti-inflammatory M2 macrophages. Thus, SHED-CM may be a novel therapeutic candidate for NP.
(徳島大学機関リポジトリ): ● Metadata: 117219
(出版サイトへのリンク): ● Publication site (DOI): 10.3389/fphar.2022.745020
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35431971; ● Summary page in Scopus @ Elsevier: 2-s2.0-85128452809

(徳島大学機関リポジトリ: 117219, DOI: 10.3389/fphar.2022.745020, PubMed: 35431971, Elsevier: Scopus) Koichi Furukawa, Yuhsuke Ohmi, Kazunori Hamamura, Yuji Kondo, Yuki Ohkawa, Kei Kaneko, Noboru Hashimoto, Farhana Yesmin, Robiul H. Bhuiyan, Orie Tajima and Keiko Furukawa :
Signaling domains of cancer-associated glycolipids.,
Glycoconjugate Journal, Vol.39, No.2, 145-155, 2022.

(要約): Immunotherapy of malignant cancers is now becoming one of representative approaches to overcome cancers. To construct strategies for immunotherapy, presence of tumor-specific antigens should be a major promise. A number of cancer specific- or cancer-associated antigens have been reported based on various experimental sets and various animal systems. The most reasonable strategy to define tumor-specific antigens might be "autologous typing" performed by Old's group, proposing three classes of tumor-antigens recognized by host immune systems of cancer patients. Namely, class 1, individual antigens that is present only in the patient's sample analyzed; class 2, shared antigens that can be found only in some group of cancers in some patients, but not in normal cells and tissues; class 3, universal antigens that are present in some cancers but also in normal cells and tissues with different densities. Sen Hakomori reported there were novel carbohydrates in cancers that could not be detected in normal cells mainly by biochemical approaches. Consequently, many of class 2 cancer-specific antigens have been revealed to be carbohydrate antigens, and been used for cancer diagnosis and treatment. Not only as cancer markers, but roles of those cancer-associated carbohydrates have also been recognized as functional molecules in cancer cells. In particular, roles of complex carbohydrates in the regulation of cell signaling on the cell surface microdomains, glycolipid-enriched microdomain (GEM)/rafts have been reported by Hakomori and many other researchers including us. The processes and present status of these studies on cancer-associated glycolipids were summarized.
(キーワード): Animals / Antigens, Tumor-Associated, Carbohydrate / Biomarkers, Tumor / Glycolipids / Humans / Neoplasms / Signal Transduction
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10719-022-10051-1
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35315508; ● Search Scopus @ Elsevier (PMID): 35315508; ● Search Scopus @ Elsevier (DOI): 10.1007/s10719-022-10051-1

(DOI: 10.1007/s10719-022-10051-1, PubMed: 35315508) Yao Liu, Linze Xia, Fumiya Kano, Noboru Hashimoto, Yoshizo Matsuka, Akihito Yamamoto and Eiji Tanaka :
Low-intensity pulsed ultrasound ameliorates neuropathic pain induced by partial sciatic nerve ligation via regulating macrophage polarization,
Journal of Oral Health and Biosciences, Vol.34, 11-18, 2021.

(徳島大学機関リポジトリ): ● Metadata: 116287
(出版サイトへのリンク): ● Publication site (DOI): 10.20738/johb.34.1_11
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390570784697431168; ● Search Scopus @ Elsevier (DOI): 10.20738/johb.34.1_11

(徳島大学機関リポジトリ: 116287, DOI: 10.20738/johb.34.1_11, CiNii: 1390570784697431168) Yuki Ohkawa, Pu Zhang, Hiroyuki Momota, Akira Kato, Noboru Hashimoto, Yuhsuke Ohmi, Robiul H. Bhuiyan, Yesmin Farhana, Atsushi Natsume, Toshihiko Wakabayashi, Keiko Furukawa and Koichi Furukawa :
Lack of GD3 synthase (St8sia1) attenuates malignant properties of gliomas in genetically engineered mouse model.,
Cancer Science, 2021.

(要約): High expression of gangliosides GD3 and GD2 is observed in human gliomas. The functions of GD3 and GD2 in malignant properties have been reported in glioma cells in vitro, but those functions have not yet been investigated in vivo. In this study, we showed that deficiency of GD3 synthase (GD3S, St8sia1) attenuated glioma progression and clinical and pathological features in a platelet-derived growth factor B-driven murine glioma model. Lack of GD3S resulted in the prolonged lifespan of glioma-bearing mice and low-grade pathology in generated gliomas. Correspondingly, they showed reduced phosphorylation levels of Akt, Erks, and Src family kinases in glioma tissues. A DNA microarray study revealed marked alteration in the expression of various genes, particularly in MMP family genes, in GD3S-deficient gliomas. Re-expression of GD3S restored expression of MMP9 in primary-cultured glioma cells. We also identified a transcription factor, Ap2α, expressed in parallel with GD3S expression, and showed that Ap2α was critical for the induction of MMP9 by transfection of its cDNA and luciferase reporter genes, and a ChIP assay. These findings suggest that GD3S enhances the progression of gliomas by enhancement of the Ap2α-MMP9 axis. This is the first report to describe the tumor-enhancing functions of GD3S in vivo.
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/cas.15032
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34145699; ● Search Scopus @ Elsevier (PMID): 34145699; ● Search Scopus @ Elsevier (DOI): 10.1111/cas.15032

(DOI: 10.1111/cas.15032, PubMed: 34145699) Naoko Ogasawara, Fumiya Kano, Noboru Hashimoto, Hiroki Mori, YAO LIU, LINZE XIA, Takuma Sakamaki, Hideharu Hibi, Tsutomu Iwamoto, Eiji Tanaka and Akihito Yamamoto :
Factors Secreted from Dental Pulp Stem Cells Show Multifaceted Benefits for Treating Experimental Temporomandibular Joint Osteoarthritis,
Osteoarthritis and Cartilage, Vol.28, No.6, 831-841, 2020.

(要約): Temporomandibular joint osteoarthritis (TMJOA) is a degenerative disease characterized by progressive cartilage degeneration, abnormal bone remodeling, and chronic pain. In this study, we aimed to investigate effective therapies to reverse or suppress TMJOA progression. To this end, we performed intravenous administration of serum free conditioned media from human exfoliated deciduous teeth stem cells (SHED-CM) into a mechanical-stress induced murine TMJOA model. SHED-CM administration markedly suppressed temporal muscle inflammation, and improved bone integrity and surface smoothness of the destroyed condylar cartilage. Moreover, SHED-CM treatment decreased the number of IL-1β, iNOS, and MMP-13 expressing chondrocytes, whereas it specifically increased PCNA-positive cells in the multipotent polymorphic cell layer. Notably, the numbers of TUNEL-positive apoptotic chondrocytes in the SHED-CM treated condyles were significantly lower than in those treated with DMEM, whereas the proteoglycan positive area was restored to a level similar to that of the sham treated group, demonstrating that SHED-CM treatment regenerated the mechanical-stress injured condylar cartilage and subchondral bone. Secretome analysis revealed that SHED-CM contained multiple therapeutic factors that act in osteochondral regeneration. Our data demonstrated that SHED-CM treatment promoted the regeneration and repair of mechanical-stress induced mouse TMJOA. Our observations suggest that SHED-CM has potential to be a potent tissue-regenerating therapeutic agent for patients with severe TMJOA.
(徳島大学機関リポジトリ): ● Metadata: 115291
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.joca.2020.03.010
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32272195; ● Search Scopus @ Elsevier (PMID): 32272195; ● Search Scopus @ Elsevier (DOI): 10.1016/j.joca.2020.03.010

(徳島大学機関リポジトリ: 115291, DOI: 10.1016/j.joca.2020.03.010, PubMed: 32272195) Koichi Furukawa, Yuhsuke Ohmi, Farhana Yesmin, Orie Tajima, Yuji Kondo, Pu Zhang, Noboru Hashimoto, Yuki Ohkawa, H. Robiul Bhuiyan and Keiko Furukawa :
Novel Molecular Mechanisms of Gangliosides in the Nervous System Elucidated by Genetic Engineering,
International Journal of Molecular Sciences, Vol.21, No.6, 1906, 2020.

(要約): Acidic glycosphingolipids, i.e., gangliosides, are predominantly and consistently expressed in nervous tissues of vertebrates at high levels. Therefore, they are considered to be involved in the development and function of nervous systems. Recent studies involving genetic engineering of glycosyltransferase genes have revealed novel aspects of the roles of gangliosides in the regulation of nervous tissues. In this review, novel findings regarding ganglioside functions and their modes of action elucidated mainly by studies of gene knockout mice are summarized. In particular, the roles of gangliosides in the regulation of lipid rafts to maintain the integrity of nervous systems are reported with a focus on the roles in the regulation of neuro-inflammation and neurodegeneration via complement systems. In addition, recent advances in studies of congenital neurological disorders due to genetic mutations of ganglioside synthase genes and also in the techniques for the analysis of ganglioside functions are introduced.
(キーワード): ganglioside / knockout / neurodegeneration / glycosphingolipid / inflammation / microdomain
(徳島大学機関リポジトリ): ● Metadata: 115632
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/ijms21061906
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050005667179691904; ● Search Scopus @ Elsevier (DOI): 10.3390/ijms21061906

(徳島大学機関リポジトリ: 115632, DOI: 10.3390/ijms21061906, CiNii: 1050005667179691904) Keita Kawarabayashi, Fumiya Kano, Noboru Hashimoto, Hideharu Hibi, Tsutomu Iwamoto and Akihito Yamamoto :
Conditioned Media from Human Dental Pulp Stem Cells Prevent Radiation-induced Skin Injury.,
Journal of Oral Health and Biosciences, Vol.33, No.1, 1-7, 2020.

(徳島大学機関リポジトリ): ● Metadata: 114712
(出版サイトへのリンク): ● Publication site (DOI): 10.20738/johb.33.1_1
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390848250116869120; ● Search Scopus @ Elsevier (DOI): 10.20738/johb.33.1_1

(徳島大学機関リポジトリ: 114712, DOI: 10.20738/johb.33.1_1, CiNii: 1390848250116869120) Noboru Hashimoto, Shizuka Ito, Akiko Tsuchida, H Robiul Bhuiyan, Tetsuya Okajima, Akihito Yamamoto, Keiko Furukawa, Yuhsuke Ohmi and Koichi Furukawa :
The ceramide moiety of disialoganglioside (GD3) is essential for GD3 recognition by the sialic acid-binding lectin SIGLEC7 on the cell surface.,
The Journal of Biological Chemistry, Vol.294, No.28, 10833-10845, 2019.

(要約): ) gene, involved in phytoceramide synthesis, disclosing that DES2 inhibition confers SIGLEC7 binding. Furthermore, knocking out fatty acid 2-hydroxylase also resulted in the emergence of SIGLEC7 binding to the cell surface. To analyze the effects of binding between SIGLEC7 and various GD3 species on natural killer function, we investigated cytotoxicity of peripheral blood mononuclear cells from healthy donors toward GD3S-transfected DLD-1 (DLD-1-GD3S) cells and DLD-1-GD3S cells with modified ceramides. We found that cytotoxicity is suppressed in DLD-1-GD3S cells with dehydroxylated GD3s. These results indicate that the ceramide structures in glycosphingolipids affect SIGLEC7 binding and distribution on the cell surface and influence cell sensitivity to killing by SIGLEC7-expressing effector cells.
(徳島大学機関リポジトリ): ● Metadata: 116450
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.RA118.007083
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31138648; ● Search Scopus @ Elsevier (PMID): 31138648; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.RA118.007083

(徳島大学機関リポジトリ: 116450, DOI: 10.1074/jbc.RA118.007083, PubMed: 31138648) Robiul H. Bhuiyan, Yuhsuke Ohmi, Yuki Ohkawa, Pu Zhang, Maiko Takano, Noboru Hashimoto, Tetsuya Okajima, Keiko Furukawa and Koichi Furukawa :
Loss of Enzyme Activity in Mutated B4GALNT1 Gene Products in Patients with Hereditary Spastic Paraplegia Results in Relatively Mild Neurological Disorders: Similarity with Phenotypes of B4galnt1 Knockout Mice.,
Neuroscience, Vol.397, 94-106, 2018.

(要約): B4GALNT1 is an enzyme essential for the synthesis of complex gangliosides, whose absence leads to progressive neurodegeneration with aging in mice. Recently, eleven cases of hereditary spastic paraplegia with mutation in the coding region of B4GALNT1 were reported. However, changes in the enzymatic activity of their products have never been studied. We have constructed expression vectors for individual mutant cDNAs, and examined their activities by cell-free in vitro enzyme assays, and flow cytometry of cells transfected with their expression vectors. Among them, almost all mutant genes showed the complete loss of B4GALNT1 activity in both the in vitro enzyme assays and flow cytometry. Two mutants exceptionally showed weak activity. One of them, M4, had a mutation at amino acid 228 with a premature termination codon. Interestingly, the intensity of fluorescence of GM2 measured by flow cytometry was equivalent between the WT and M4 mutant, although the positive cell population was relatively small in M4. Western immunoblotting of cell lysates from transfectants with cDNA plasmids revealed 67-kDa bands except those containing premature termination codons or frame-shift mutation. Taken together with the clinical findings of patients, loss of enzyme activity may be responsible for the clinical features of hereditary spastic paraplegia, whereas the intensity of neurological disorders was relatively milder than expected. These clinical features of patients including those with male hypogonadism are very similar to the abnormal phenotypes detected in B4galnt1-deficient mice.
(キーワード): Animals / CHO Cells / Cell Line, Tumor / Cricetulus / Disease Models, Animal / HEK293 Cells / Humans / Mice, Knockout / Mutation / N-Acetylgalactosaminyltransferases / Phenotype / Spastic Paraplegia, Hereditary
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.neuroscience.2018.11.034
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30521973; ● Search Scopus @ Elsevier (PMID): 30521973; ● Search Scopus @ Elsevier (DOI): 10.1016/j.neuroscience.2018.11.034

(DOI: 10.1016/j.neuroscience.2018.11.034, PubMed: 30521973) Koichi Furukawa, Yuhsuke Ohmi, Orie Tajima, Yuki Ohkawa, Yuji Kondo, Ji Shuting, Noboru Hashimoto and Keiko Furukawa :
Gangliosides in Inflammation and Neurodegeneration.,
Progress in Molecular Biology and Translational Science, Vol.156, 265-287, 2018.

(要約): Gangliosides play roles in the regulation of cell signaling that are mediated via membrane microdomains, lipid rafts. In this review, functions of gangliosides in the maintenance of nervous systems with a focus on regulation of inflammation and neurodegeneration are addressed. During analyses of various ganglioside-lacking mutant mice, we demonstrated that nervous tissues exhibited inflammatory reactions and subsequent neurodegeneration. Among inflammation-related genes, factors of the complement system showed up-regulation with aging. Analyses of architectures and compositions of lipid rafts in nervous tissues from these mutant mice revealed that dysfunctions of complement regulatory proteins based on disrupted lipid rafts were main factors to induce the inflammatory reactions resulting in neurodegeneration. Ganglioside changes in development and senescence, and implication of them in the integrity of cell membranes and cellular phenotypes in physiological and pathological conditions including Alzheimer disease have been summarized. Novel directions to further analyze mechanisms for ganglioside functions in membrane microdomains have been also addressed.
(キーワード): Animals / Gangliosides / Humans / Inflammation / Neurodegenerative Diseases
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/bs.pmbts.2018.01.009
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29747817; ● Search Scopus @ Elsevier (PMID): 29747817; ● Search Scopus @ Elsevier (DOI): 10.1016/bs.pmbts.2018.01.009

(DOI: 10.1016/bs.pmbts.2018.01.009, PubMed: 29747817) Nobutoshi Esaki, Yuki Ohkawa, Noboru Hashimoto, Yuhsuke Tsuda, Yuhsuke Ohmi, Robiul H. Bhuiyan, Norihiro Kotani, Koichi Honke, Atsushi Enomoto, Masahide Takahashi, Keiko Furukawa and Koichi Furukawa :
ASC amino acid transporter 2, defined by enzyme-mediated activation of radical sources, enhances malignancy of GD2-positive small-cell lung cancer.,
Cancer Science, Vol.109, No.1, 141-153, 2018.

(要約): Ganglioside GD2 is specifically expressed in small-cell lung cancer (SCLC) cells, leading to enhancement of malignant phenotypes, such as cell proliferation and migration. However, how GD2 promotes malignant phenotypes in SCLC cells is not well known. In this study, to reveal the mechanisms by which GD2 increases malignant phenotypes in SCLC cells, we used enzyme-mediated activation of radical sources combined with mass spectrometry in GD2 SCLC cells. Consequently, we identified ASC amino acid transporter 2 (ASCT2), a major glutamine transporter, which coordinately works with GD2. We showed that ASCT2 was highly expressed in glycolipid-enriched microdomain/rafts in GD2 SCLC cells, and colocalized with GD2 in both proximity ligation assay and immunocytostaining, and bound with GD2 in immunoprecipitation/TLC immunostaining. Malignant phenotypes of GD2 SCLC cells were enhanced by glutamine uptake, and were suppressed by L-γ-glutamyl-p-nitroanilide, a specific inhibitor of ASCT2, through reduced phosphorylation of p70 S6K1 and S6. These results suggested that ASCT2 enhances glutamine uptake in glycolipid-enriched microdomain/rafts in GD2 SCLC cells, leading to the enhancement of cell proliferation and migration through increased phosphorylation of the mTOR complex 1 signaling axis.
(キーワード): Amino Acid Transport System ASC / Cell Line, Tumor / Cell Movement / Cell Proliferation / Gangliosides / Glutamine / Humans / Lung Neoplasms / Membrane Microdomains / Minor Histocompatibility Antigens / Small Cell Lung Carcinoma
(徳島大学機関リポジトリ): ● Metadata: 117756
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/cas.13448
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29151270; ● Search Scopus @ Elsevier (PMID): 29151270; ● Search Scopus @ Elsevier (DOI): 10.1111/cas.13448

(徳島大学機関リポジトリ: 117756, DOI: 10.1111/cas.13448, PubMed: 29151270) Koichi Furukawa, Yuhsuke Ohmi, Shuting Ji, Pu Zhang, Robiul H. Bhuiyan, Yuki Ohkawa, Orie Tajima, Noboru Hashimoto and Keiko Furukawa :
Glycolipids: Essential regulator of neuro-inflammation, metabolism and gliomagenesis.,
Biochimica et Biophysica Acta (BBA) - General Subjects, Vol.1861, No.10, 2479-2484, 2017.

(要約): Gene knockout mice of glycosyltransferases have clearly showed roles of their products in the bodies, while there are examples where phenotype of knockout was much less severe than expected probably due to functional redundancy. The most striking novel finding obtained from ganglioside-deficient mice was that progressive inflammatory reaction took place, leading to neurodegeneration. In particular, dysfunction of complement-regulatory proteins due to deteriorated architecture of lipid rafts seemed to be essential mechanisms for the inflammation. Furthermore, roles of gangliosides in neurons were demonstrated by neuron-specific transgenic of B4galnt1 with genetic background of B4galnt1 deficiency. From study of gene knockout mice of St8sia1, new roles of b-series gangliosides in leptin secretion from adipocytes, and roles of a-series gangliosides in leptin receptor, ObR in hypothalamus were demonstrated, leading to apparent intact balance of energy. Essential roles of b-series gangliosides in malignant properties of gliomas were also shown, suggesting their roles in the regulation of inflammation and proliferation in nervous tissues. How to apply these findings for the control of newly discovered patients with ganglioside deficiency remains to be investigated. This article is part of a Special Issue entitled Neuro-glycoscience, edited by Kenji Kadomatsu and Hiroshi Kitagawa.
(キーワード): Animals / Complement System Proteins / Gangliosides / Gene Expression Regulation, Neoplastic / Glioma / Humans / Inflammation / Leptin / Membrane Microdomains / Mice / Mice, Knockout / N-Acetylgalactosaminyltransferases / Neoplasms, Nerve Tissue / Nerve Tissue / Neurons / Receptors, Leptin / Sialyltransferases
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbagen.2017.06.007
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28602513; ● Search Scopus @ Elsevier (PMID): 28602513; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbagen.2017.06.007

(DOI: 10.1016/j.bbagen.2017.06.007, PubMed: 28602513) Kei Kaneko, Yuki Ohkawa, Noboru Hashimoto, Yuhsuke Ohmi, Norihiro Kotani, Koichi Honke, Mitsutaka Ogawa, Tetsuya Okajima, Keiko Furukawa and Koichi Furukawa :
Neogenin, Defined as a GD3-associated Molecule by Enzyme-mediated Activation of Radical Sources, Confers Malignant Properties via Intracytoplasmic Domain in Melanoma Cells.,
The Journal of Biological Chemistry, Vol.291, No.32, 16630-16643, 2016.

(要約): To investigate mechanisms for increased malignant properties in malignant melanomas by ganglioside GD3, enzyme-mediated activation of radical sources and subsequent mass spectrometry were performed using an anti-GD3 antibody and GD3-positive (GD3+) and GD3-negative (GD3-) melanoma cell lines. Neogenin, defined as a GD3-neighbored molecule, was largely localized in lipid/rafts in GD3+ cells. Silencing of neogenin resulted in the reduction of cell growth and invasion activity. Physical association between GD3 and neogenin was demonstrated by immunoblotting of the immunoprecipitates with anti-neogenin antibody from GD3+ cell lysates. The intracytoplasmic domain of neogenin (Ne-ICD) was detected in GD3+ cells at higher levels than in GD3- cells when cells were treated by a proteasome inhibitor but not when simultaneously treated with a γ-secretase inhibitor. Exogenous GD3 also induced increased Ne-ICD in GD3- cells. Overexpression of Ne-ICD in GD3- cells resulted in the increased cell growth and invasion activity, suggesting that Ne-ICD plays a role as a transcriptional factor to drive malignant properties of melanomas after cleavage with γ-secretase. γ-Secretase was found in lipid/rafts in GD3+ cells. Accordingly, immunocyto-staining revealed that GD3, neogenin, and γ-secretase were co-localized at the leading edge of GD3+ cells. All these results suggested that GD3 recruits γ-secretase to lipid/rafts, allowing efficient cleavage of neogenin. ChIP-sequencing was performed to identify candidates of target genes of Ne-ICD. Some of them actually showed increased expression after expression of Ne-ICD, probably exerting malignant phenotypes of melanomas under GD3 expression.
(キーワード): Amyloid Precursor Protein Secretases / Cell Line, Tumor / Gangliosides / Gene Expression Regulation, Neoplastic / Humans / Melanoma / Membrane Microdomains / Neoplasm Proteins / Nerve Tissue Proteins / Receptors, Cell Surface
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.M115.708834
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27288875; ● Search Scopus @ Elsevier (PMID): 27288875; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M115.708834

(DOI: 10.1074/jbc.M115.708834, PubMed: 27288875) Hasan Robiul Bhuiyan, Yuji Kondo, Tokiaki Yamaguchi, Noriyo Tokuda, Yuki Ohkawa, Noboru Hashimoto, Yuhsuke Ohmi, Yoshio Yamauchi, Keiko Furukawa, Tetsuya Okajima and Koichi Furukawa :
Expression analysis of 0-series gangliosides in human cancer cell lines with monoclonal antibodies generated using knockout mice of ganglioside synthase genes.,
Glycobiology, Vol.26, No.9, 984-998, 2016.

(要約): Some gangliosides, sialic acid-containing glycosphingolipids, have been considered as tumor-associated antigens. GD1α or a GD1α synthase gene ST6GalNAc5 was reported to be involved in the metastasis of murine lymphomas or human breast cancers, respectively. But expression patterns of 0-series gangliosides GD1α and its precursor GM1b in human cancers have not yet been investigated mainly due to lack of specific antibodies. We established specific monoclonal antibodies (mAbs) reactive with GD1α or GM1b using gangliosides from brain tissues of GM3 synthase (St3gal5)-deficient mice as immunogens. We used GM2/GD2 synthase (B4galnt1)-deficient mice to immunize by liposomes embedded with GD1α or acidic glycolipid fractions from brain of St3gal5-deficient mice. Specificities of established mAbs as analyzed by enzyme-linked immunosorbent assay and thin-layer chromatography-immunostaining were very high among various gangliosides. Increased expression of GD1α and reduced GM1b in the St6galnac5 cDNA-transfected RAW117 cell line also substantiated the specificities of two mAbs. Then, we analyzed expression of GD1α and GM1b, and of relevant glycosyltransferase genes in various human cancer cell lines using generated anti-GD1α mAb 122 or anti-GM1b mAb MR155A-7. A few human cancer cell lines showed significant expression of these gangliosides with reasonable expression of relevant glycosyltransferase genes.
(キーワード): Animals / Antibodies, Monoclonal / Antigens, Neoplasm / Cell Line, Tumor / G(M1) Ganglioside / Gangliosides / Gene Expression Regulation, Enzymologic / Glycosphingolipids / Humans / ノックアウトマウス (knockout mice) / N-Acetylgalactosaminyltransferases / Neoplasm Metastasis / Sialyltransferases
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/glycob/cww049
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27102283; ● Search Scopus @ Elsevier (PMID): 27102283; ● Search Scopus @ Elsevier (DOI): 10.1093/glycob/cww049

(DOI: 10.1093/glycob/cww049, PubMed: 27102283) Reiko Ando, Noriyo Tokuda, Tokunori Yamamoto, Kazutaka Ikeda, Noboru Hashimoto, Ryo Taguchi, Xiaoen Fan, Keiko Furukawa, Yukio Niimura, Akemi Suzuki, Momokazu Goto and Koichi Furukawa :
Immunization of A4galt-deficient mice with glycosphingolipids from renal cell cancers resulted in the generation of anti-sulfoglycolipid monoclonal antibodies.,
Glycoconjugate Journal, Vol.33, No.2, 169-180, 2016.

(要約): In this study, we immunized Gb3/CD77 synthase gene (A4galt) knockout (KO) mice with glycosphingolipids (GSLs) extracted from 3 renal cell cancer (RCC) cell lines to raise monoclonal antibodies (mAbs) reactive with globo-series GSLs specifically expressed in RCCs. Although a number of mAbs reactive with globo-series GSLs were generated, they reacted with both RCC cell lines and normal kidney cells. When we analyzed recognized antigens by mAbs that were specifically reactive with RCC, but not with normal kidney cells at least on the cell surface, many of them turned out to be reactive with sulfoglycolipids. Eight out of 11 RCC-specific mAbs were reactive with SM2 alone, and the other 3 mAbs were more broadly reactive with sulfated glycolipids, i.e. SM3 and SM4 as well as SM2. In the immunohistochemistry, these anti-sulfoglycolipids mAbs showed RCC-specific reaction, with no or minimal reaction with adjacent normal tissues. Thus, immunization of A4galt KO mice with RCC-derived GSLs resulted in the generation of anti sulfated GSL mAbs, and these mAbs may be applicable for the therapeutics for RCC patients.
(キーワード): Animals / Antibodies, Monoclonal, Murine-Derived / Antibodies, Neoplasm / Cell Line, Tumor / Galactosyltransferases / Glycolipids / Humans / Immunization / Kidney Neoplasms / ノックアウトマウス (knockout mice)
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10719-016-9654-6
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26883028; ● Search Scopus @ Elsevier (PMID): 26883028; ● Search Scopus @ Elsevier (DOI): 10.1007/s10719-016-9654-6

(DOI: 10.1007/s10719-016-9654-6, PubMed: 26883028) Yuki Ohkawa, Hiroyuki Momota, Akira Kato, Noboru Hashimoto, Yusuke Tsuda, Norihiro Kotani, Koichi Honke, Akio Suzumura, Keiko Furukawa, Yuhsuke Ohmi, Atsushi Natsume, Toshihiko Wakabayashi and Koichi Furukawa :
Ganglioside GD3 Enhances Invasiveness of Gliomas by Forming a Complex with Platelet-derived Growth Factor Receptor α and Yes Kinase.,
The Journal of Biological Chemistry, Vol.290, No.26, 16043-16058, 2015.

(要約): There have been a few studies on the ganglioside expression in human glioma tissues. However, the role of these gangliosides such as GD3 and GD2 has not been well understood. In this study we employed a genetically engineered mouse model of glioma to clarify the functions of GD3 in gliomas. Forced expression of platelet-derived growth factor B in cultured astrocytes derived from p53-deficient mice resulted in the expression of GD3 and GD2. GD3-positive astrocytes exhibited increased cell growth and invasion activities along with elevated phosphorylation of Akt and Yes kinase. By enzyme-mediated activation of radical sources reaction and mass spectrometry, we identified PDGF receptor α (PDGFRα) as a GD3-associated molecule. GD3-positive astrocytes showed a significant amount of PDGFRα in glycolipid-enriched microdomains/rafts compared with GD3-negative cells. Src kinase family Yes was co-precipitated with PDGFRα, and its pivotal role in the increased cell invasion of GD3-positive astrocytes was demonstrated by silencing with anti-Yes siRNA. Direct association between PDGFRα and GD3 was also shown, suggesting that GD3 forms ternary complex with PDGFRα and Yes. The fact that GD3, PDGFRα, and activated Yes were colocalized in lamellipodia and the edge of tumors in cultured cells and glioma tissues, respectively, suggests that GD3 induced by platelet-derived growth factor B enhances PDGF signals in glycolipid-enriched microdomain/rafts, leading to the promotion of malignant phenotypes such as cell proliferation and invasion in gliomas.
(キーワード): Animals / Brain Neoplasms / Gangliosides / Glioma / Humans / Mice / Neoplasm Invasiveness / Protein Binding / Proto-Oncogene Proteins c-yes / Receptor, Platelet-Derived Growth Factor alpha
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.M114.635755
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25940087; ● Search Scopus @ Elsevier (PMID): 25940087; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M114.635755

(DOI: 10.1074/jbc.M114.635755, PubMed: 25940087) Kohki Matsubara, Yoshihiro Matsushita, Kiyoshi Sakai, Fumiya Kano, Megumi Kondo, Mariko Noda, Noboru Hashimoto, Shiro Imagama, Naoki Ishiguro, Akio Suzumura, Minoru Ueda, Koichi Furukawa and Akihito Yamamoto :
Secreted ectodomain of sialic acid-binding Ig-like lectin-9 and monocyte chemoattractant protein-1 promote recovery after rat spinal cord injury by altering macrophage polarity.,
The Journal of Neuroscience, Vol.35, No.6, 2452-2464, 2015.

(要約): Engrafted mesenchymal stem cells from human deciduous dental pulp (SHEDs) support recovery from neural insults via paracrine mechanisms that are poorly understood. Here we show that the conditioned serum-free medium (CM) from SHEDs, administered intrathecally into rat injured spinal cord during the acute postinjury period, caused remarkable functional recovery. The ability of SHED-CM to induce recovery was associated with an immunoregulatory activity that induced anti-inflammatory M2-like macrophages. Secretome analysis of the SHED-CM revealed a previously unrecognized set of inducers for anti-inflammatory M2-like macrophages: monocyte chemoattractant protein-1 (MCP-1) and the secreted ectodomain of sialic acid-binding Ig-like lectin-9 (ED-Siglec-9). Depleting MCP-1 and ED-Siglec-9 from the SHED-CM prominently reduced its ability to induce M2-like macrophages and to promote functional recovery after spinal cord injury (SCI). The combination of MCP-1 and ED-Siglec-9 synergistically promoted the M2-like differentiation of bone marrow-derived macrophages in vitro, and this effect was abolished by a selective antagonist for CC chemokine receptor 2 (CCR2) or by the genetic knock-out of CCR2. Furthermore, MCP-1 and ED-Siglec-9 administration into the injured spinal cord induced M2-like macrophages and led to a marked recovery of hindlimb locomotor function after SCI. The inhibition of this M2 induction through the inactivation of CCR2 function abolished the therapeutic effects of both SHED-CM and MCP-1/ED-Siglec-9. Macrophages activated by MCP-1 and ED-Siglec-9 extended neurite and suppressed apoptosis of primary cerebellar granule neurons against the neurotoxic effects of chondroitin sulfate proteoglycans. Our data suggest that the unique combination of MCP-1 and ED-Siglec-9 repairs the SCI through anti-inflammatory M2-like macrophage induction.
(キーワード): Animals / Antigens, CD / 血液脳関門 (blood-brain barrier) / Brain Injuries / Cell Polarity / 小脳 (cerebellum) / Chemokine CCL2 / Child / Culture Media, Conditioned / Cytokines / Dental Pulp / Humans / Macrophages / Mice / Mice, Inbred C57BL / Rats / Rats, Sprague-Dawley / Receptors, CCR2 / Sialic Acid Binding Immunoglobulin-like Lectins / Spinal Cord Injuries / Tooth, Deciduous
(出版サイトへのリンク): ● Publication site (DOI): 10.1523/JNEUROSCI.4088-14.2015
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25673840; ● Summary page in Scopus @ Elsevier: 2-s2.0-84922553212

(DOI: 10.1523/JNEUROSCI.4088-14.2015, PubMed: 25673840, Elsevier: Scopus) Ilhamjan Sabit, Noboru Hashimoto, Yasuyuki Matsumoto, Toshiyuki Yamaji, Keiko Furukawa and Koichi Furukawa :
Binding of a sialic acid-recognizing lectin Siglec-9 modulates adhesion dynamics of cancer cells via calpain-mediated protein degradation.,
The Journal of Biological Chemistry, Vol.288, No.49, 35417-35427, 2013.

(要約): Although regulatory mechanisms for immune cells with inhibitory signals via immunoreceptor tyrosine-based inhibitory motifs are well known, signals transduced via interaction between Siglecs and sialyl compounds on their counterreceptors into target cells have not been reported to date. In this study, we found that an astrocytoma cell line, AS, showed detachment from culture plates when co-cultured with Siglec-9-expressing cells and/or soluble Siglec-9. Moreover, detached AS cells regrew as co-cultured cells with Siglec-9-deficient cells. They also showed increased motility and invasiveness upon Siglec-9 binding. In immunoblotting, rapid degradation of focal adhesion kinase (FAK) and related signaling molecules such as Akt, paxillin, and p130Cas was observed immediately after the co-culture. Despite degradation of these molecules, increased p-Akt was found at the front region of the cytoplasm, probably reflecting increased cell motility. Calpain was considered to be a responsible protease for the protein degradation by the inhibition experiments. These results suggest that protein degradation of FAK and related molecules was induced by Siglec-9 binding to its counterreceptors via sialylglycoconjugates, leading to the modulation of adhesion kinetics of cancer cells. Thus, this might be a mechanism by which cancer cells utilize Siglec-9-derived signals to escape from immunosurveillance.
(キーワード): Antigens, CD / Calpain / Cell Adhesion / Cell Line, Tumor / Focal Adhesion Kinase 1 / Humans / Neoplasm Proteins / Neoplasms / Protein Binding / Receptors, Mitogen / Sialic Acid Binding Immunoglobulin-like Lectins / シグナル伝達 (signal transduction) / U937 Cells
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.M113.513192
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24145038; ● Search Scopus @ Elsevier (PMID): 24145038; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M113.513192

(DOI: 10.1074/jbc.M113.513192, PubMed: 24145038) Noriyo Tokuda, Shinichiro Numata, Xiaojin Li, Tomoko Nomura, Minoru Takizawa, Yuji Kondo, Yoriko Yamashita, Noboru Hashimoto, Tohru Kiyono, Takeshi Urano, Keiko Furukawa and Koichi Furukawa :
β4GalT6 is involved in the synthesis of lactosylceramide with less intensity than β4GalT5.,
Glycobiology, Vol.23, No.10, 1175-1183, 2013.

(要約): Glycosphingolipids are expressed on the cell membrane and act as important factors in various events that occur across the plasma membrane. Lactosylceramide (LacCer) is synthesized from glucosylceramide and is a common precursor of various glycosphingolipids existing in whole body. Based on the enzyme purification, β1,4-galactosyltransferase 6 (B4galt6) cDNA was isolated as a LacCer synthase-coding gene in the rat brain. We generated B4galt6 gene knockout (KO) mice and analyzed their phenotypes to examine roles of β4GalT6. B4galt6 KO mice were born and grew up apparently normal. LacCer synthase activity and the composition of acidic glycosphingolipids in the brain were almost equivalent or minimally different between wild-type and KO mice. Studies by mouse embryonic fibroblasts (MEFs) revealed that the silencing of B4galt5 gene resulted in the marked reduction in LacCer synthase activity and this reduction was more severe in MEFs derived from B4galt6 KO mice than those from wild-type mice. These results suggested that β4GalT6 plays a role as a LacCer synthase, whereas β4GalT5 acts as a main enzyme for LacCer biosynthesis in these tissues and cells.
(キーワード): Animals / Brain / Cell Line / Galactosyltransferases / Lactosylceramides / Mice / Mice, Inbred C57BL / Mice, Knockout / Phenotype
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/glycob/cwt054
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23882130; ● Search Scopus @ Elsevier (PMID): 23882130; ● Search Scopus @ Elsevier (DOI): 10.1093/glycob/cwt054

(DOI: 10.1093/glycob/cwt054, PubMed: 23882130) Hiroshi Hotta, Kazunori Hamamura, Kyoko Yamashita, Hidenobu Shibuya, Noriyo Tokuda, Noboru Hashimoto, Keiko Furukawa, Noriyuki Yamamoto, Hisashi Hattori, Shinya Toyokuni, Minoru Ueda and Koichi Furukawa :
Lewis y antigen is expressed in oral squamous cell carcinoma cell lines and tissues, but disappears in the invasive regions leading to the enhanced malignant properties irrespective of sialyl-Lewis x.,
Glycoconjugate Journal, Vol.30, No.6, 585-597, 2012.

(要約): Expression and implication of carbohydrate antigens in squamous cell carcinomas (SCCs) in oral cavity was examined. In the cell lines, type 2H and Lewis y antigens were markedly expressed. In the tissues from SCC patients and benign disorders, type 2H was highly expressed in hyperplasia (96.4 %), displasia (92.9 %) and SCC (100 %). Lewis y was, in turn, expressed mainly in cancer tissues (91.3 %), suggesting that Lewis y is a cancer-associated antigen. Normal oral mucosa showed no expression of these blood group antigens. Surprisingly, Lewis y antigen disappeared in the invasion sites where Ki-67 was definitely stained. Over-expression of Lewis y with manipulation of a fucosyltransferase cDNA resulted in suppression of cell growth and invasion, and knockdown of Lewis y also brought about increased cell growth and invasion. In either situations, no changes in the expression of sialyl-Lewis x could be found. Lowered tumor growth and invasion into surrounding tissues were also shown in Lewis y-positive SCC grafts in nu/nu mice. All these results together with alternative staining between Lewis y and Ki-67 in cancer tissues and FUT1 transfectants suggested that loss of Lewis y is a crucial event for the late stage of SCCs.
(キーワード): Animals / Carcinoma, Squamous Cell / Cell Line, Tumor / Fucosyltransferases / Gene Expression Regulation, Neoplastic / Humans / Ki-67 Antigen / Lewis Blood Group Antigens / Mice, Inbred BALB C / Mouth Mucosa / Mouth Neoplasms / Neoplasm Invasiveness / Neoplasm Transplantation / Oligosaccharides / Organ Specificity / Sialyl Lewis X Antigen
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10719-012-9458-2
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23242548; ● Search Scopus @ Elsevier (PMID): 23242548; ● Search Scopus @ Elsevier (DOI): 10.1007/s10719-012-9458-2

(DOI: 10.1007/s10719-012-9458-2, PubMed: 23242548) Maiko Kurosawa, D Anand Jeyasekharan, Eva-Maria Surmann, Noboru Hashimoto, Vignesh Venkatraman, Gene Kurosawa, Koichi Furukawa, R Ashok Venkitaraman and Yoshikazu Kurosawa :
Expression of LY6D is induced at the surface of MCF10A cells by X-ray irradiation.,
The FEBS Journal, Vol.279, No.24, 4479-4491, 2012.

(要約): In order to identify membrane proteins whose expression is induced by X-ray irradiation, we developed an antibody (Ab)-directed strategy using a phage Ab library. X-Ray-irradiated cells were screened with a phage Ab library in the presence of a large excess of polyclonal Abs prepared against membrane proteins that are commonly present at the surface of both X-ray-irradiated and nonirradiated cells. After isolation of Ab that bound only to X-ray-irradiated cells, the antigen was identified using MS. Using this approach, we found that expression of LY6D is induced in MCF10A cells by X-ray irradiation. The induction of LY6D expression is triggered through a pathway regulated by ATM, CHK2 and p53. This method is a new Ab-directed proteomic strategy for analysis of membrane proteins, and is applicable to various biological phenomena in situations in which both target molecule-expressing cells and nonexpressing cells are available.
(キーワード): Ataxia Telangiectasia Mutated Proteins / Base Sequence / Cell Adhesion Molecules / Cell Cycle Proteins / Cell Line, Tumor / Checkpoint Kinase 2 / DNA Primers / DNA-Binding Proteins / GPI-Linked Proteins / Humans / Mutagens / Protein-Serine-Threonine Kinases / Proto-Oncogene Proteins p21(ras) / RNA, Small Interfering / Real-Time Polymerase Chain Reaction / Transcription, Genetic / Tumor Suppressor Protein p53 / Tumor Suppressor Proteins / X-Rays
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/febs.12034
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23075424; ● Search Scopus @ Elsevier (PMID): 23075424; ● Search Scopus @ Elsevier (DOI): 10.1111/febs.12034

(DOI: 10.1111/febs.12034, PubMed: 23075424) Noboru Hashimoto, Kazunori Hamamura, Norihiro Kotani, Keiko Furukawa, Kei Kaneko, Koichi Honke and Koichi Furukawa :
Proteomic analysis of ganglioside-associated membrane molecules: substantial basis for molecular clustering.,
Proteomics, Vol.12, No.21, 3154-3163, 2012.

(要約): Ganglioside GD3 is specifically expressed in human melanomas, and plays a role in the enhancement of malignant phenotypes of melanoma cells. To analyze the mechanisms by which GD3 enhances malignant properties and signals in melanomas, it is essential to clarify how GD3 interacts with membrane molecules on the cell membrane. In this study, we performed proteomics analysis of glycolipid-enriched microdomains (GEM) with current sucrose density gradient ultracentrifugation of Triton X-100 extracts and MS. We also examined GD3-associated molecules using enzyme-mediated activation of radical sources (EMARS) reaction combined with MS. Comparison of molecules identified as residents in GEM/rafts and those detected by EMARS reaction using an anti-GD3 antibody revealed that a relatively low number of molecules is recruited around GD3, while a number of membrane and secreted molecules was defined in GEM/rafts. These results suggested that EMARS reaction is useful to identify actually interacting molecules with gangliosides such as GD3 on the cell membrane, and many other microdomains than GD3-associating rafts exist. Representative examples of GD3-associated molecules such as neogenin and MCAM were shown.
(キーワード): Cell Line, Tumor / Gangliosides / Humans / 質量分析法 (mass spectrometry) / Melanoma / Membrane Microdomains / Membrane Proteins / プロテオーム (proteome) / プロテオミクス (proteomics)
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/pmic.201200279
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22936677; ● Search Scopus @ Elsevier (PMID): 22936677; ● Search Scopus @ Elsevier (DOI): 10.1002/pmic.201200279

(DOI: 10.1002/pmic.201200279, PubMed: 22936677) Kazunori Hamamura, Momoko Tsuji, Hiroshi Hotta, Yuki Ohkawa, Masataka Takahashi, Hidenobu Shibuya, Hideyuki Nakashima, Yoshio Yamauchi, Noboru Hashimoto, Hisashi Hattori, Minoru Ueda, Keiko Furukawa and Koichi Furukawa :
Functional activation of Src family kinase yes protein is essential for the enhanced malignant properties of human melanoma cells expressing ganglioside GD3.,
The Journal of Biological Chemistry, Vol.286, No.21, 18526-18537, 2011.

(要約): The possible roles of Src family kinases in the enhanced malignant properties of melanomas related to GD3 expression were analyzed. Among Src family kinases only Yes, not Fyn or Src, was functionally involved in the increased cell proliferation and invasion of GD3-expressing transfectant cells (GD3+). Yes was located upstream of p130Cas and paxillin and at an equivalent level to focal adhesion kinase. Yes underwent autophosphorylation even before serum treatment and showed stronger kinase activity in GD3+ cells than in GD3- cells following serum treatment. Coimmunoprecipitation experiments revealed that Yes bound to focal adhesion kinase or p130Cas more strongly in GD3+ cells than in GD3- cells. As a possible mechanism for the enhancing effects of GD3 on cellular phenotypes, it was shown that majority of Yes was localized in glycolipid-enriched microdomain/rafts in GD3+ cells even before serum treatment, whereas it was scarcely detected in glycolipid-enriched microdomain/rafts in GD3- cells. An in vitro kinase assay of Yes revealed that coexistence of GD3 with Yes in membranous environments enhances the kinase activity of GD3- cell-derived Yes toward enolase, p125, and Yes itself. Knockdown of GD3 synthase resulted in the alleviation of tumor phenotypes and reduced activation levels of Yes. Taken together, these results suggest a role of GD3 in the regulation of Src family kinases.
(キーワード): Cell Line, Tumor / Crk-Associated Substrate Protein / Enzyme Activation / Focal Adhesion Protein-Tyrosine Kinases / Gangliosides / Gene Expression Regulation, Neoplastic / Gene Knockdown Techniques / Humans / Melanoma / Membrane Microdomains / Phosphopyruvate Hydratase / Proto-Oncogene Proteins c-yes / Sialyltransferases
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.M110.164798
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21454696; ● Search Scopus @ Elsevier (PMID): 21454696; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M110.164798

(DOI: 10.1074/jbc.M110.164798, PubMed: 21454696) Tomita Makoto, Noboru Hashimoto and Tanaka Yutaka :
Association study for the relationship between a haplotype or haplotype set and multiple quantitative responses,
Computational Statistics & Data Analysis, Vol.55, No.6, 2104-2113, 2011.

(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.csda.2011.01.002
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-79952039391

(DOI: 10.1016/j.csda.2011.01.002, Elsevier: Scopus)

MISC

研究者総覧に該当データはありませんでした。

総説・解説

Eiji Tanaka, YAO LIU, LINZE XIA, Naoko Ogasawara, Takuma Sakamaki, Fumiya Kano, Noboru Hashimoto, Xingmei Feng and Akihito Yamamoto :
Effectiveness of low-intensity pulsed ultrasound on osteoarthritis of the temporomandibular joint: A review.,
Annals of Biomedical Engineering, Vol.48, No.8, 2158-2170, Jun. 2020.

(要約): Loading is indispensable for the growth, development, and maintenance of joint tissues, including mandibular condylar cartilage, but excessive loading or reduced host adaptive capacity can considerably damage the temporomandibular joint (TMJ), leading to temporomandibular joint osteoarthritis (TMJ-OA). TMJ-OA, associated with other pathological conditions and aging processes, is a highly degenerative disease affecting the articular cartilage. Many treatment modalities for TMJ-OA have been developed. Traditional clinical treatment includes mainly nonsurgical options, such as occlusal splints. However, non-invasive therapy does not achieve joint tissue repair and regeneration. Growing evidence suggests that low-intensity pulsed ultrasound (LIPUS) accelerates bone fracture healing and regeneration, as well as having extraordinary effects in terms of soft tissue repair and regeneration. The latter have received much attention, and various studies have been performed to evaluate the potential role of LIPUS in tissue regeneration including that applied to articular cartilage. The present article provides an overview of the status of LIPUS stimulation used to prevent the onset and progression of TMJ-OA and enhance the tissue regeneration of mandibular condylar cartilage. The etiology and management of TMJ-OA are explained briefly, animal models of TMJ-OA are described, and the effectiveness of LIPUS on cell metabolism and tissue regeneration in the TMJ is discussed.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10439-020-02540-x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32514932; ● Search Scopus @ Elsevier (PMID): 32514932; ● Search Scopus @ Elsevier (DOI): 10.1007/s10439-020-02540-x

(DOI: 10.1007/s10439-020-02540-x, PubMed: 32514932) Koichi Furukawa, Yuhsuke Ohmi, Yuki Ohkawa, Robiul H. Bhuiyan, Pu Zhang, Orie Tajima, Noboru Hashimoto, Kazunori Hamamura and Keiko Furukawa :
New era of research on cancer-associated glycosphingolipids.,
Cancer Science, Vol.110, No.5, 1544-1551, Apr. 2019.

(要約): Cancer-associated glycosphingolipids have been used as markers for diagnosis and targets for immunotherapy of malignant tumors. Recent progress in the analysis of their implications in the malignant properties of cancer cells revealed that cancer-associated glycosphingolipids are not only tumor markers, but also functional molecules regulating various signals introduced by membrane microdomains, lipid rafts. In particular, a novel approach, enzyme-mediated activation of radical sources combined with mass spectrometry, has enabled us to clarify the mechanisms by which cancer-associated glycosphingolipids regulate cell signals based on the interaction with membrane molecules and formation of molecular complexes on the cell surface. Novel findings obtained from these approaches are now providing us with insights into the development of new anticancer therapies targeting membrane molecular complexes consisting of cancer-associated glycolipids and their associated membrane molecules. Thus, a new era of cancer-associated glycosphingolipids has now begun.
(キーワード): Animals / Biomarkers, Tumor / Cell Membrane / Glycosphingolipids / Humans / Mass Spectrometry / Neoplasms / Signal Transduction
(徳島大学機関リポジトリ): ● Metadata: 114571
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/cas.14005
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30895683; ● Search Scopus @ Elsevier (PMID): 30895683; ● Search Scopus @ Elsevier (DOI): 10.1111/cas.14005

(徳島大学機関リポジトリ: 114571, DOI: 10.1111/cas.14005, PubMed: 30895683)

講演・発表

Noboru Hashimoto, Ito Shizuka, Ikeda Kazutaka, Tsuchida Akiko, Crocker R. Paul, Furukawa Keiko, Taguchi Ryo and Furukawa Koichi :
Structural specificity in molecular recognition of Siglec-7 to ganglioside GD3,
Gordon Reserch Conference Glycolipid &Sphingolipid Biology, Lucca (Barga), Italy, Mar. 2016. Noboru Hashimoto, Kazunori Hamamura, Norihiro Kotani, Keiko Furukawa, Kei Kaneko, Koichi Honke and Koichi Furukawa :
Proteomic analysis of ganglioside-associated microdomain in malignant melanomas.,
2014 SFG & JSCR JOINT MEETING, Honolulu, Nov. 2014. Noboru Hashimoto :
Proteomics of ganglioside GD3-containing microdomains in malignant melanomas,
Gordon Reserch Conference Glycolipid & Sphingolipid Biology, Ventura, CA, Jan. 2014. Noboru Hashimoto, Hamamura Kazunori, Kotani Norihiro, Ohkawa Yuki, Furukawa Keiko, Honke Koichi and Furukawa Koichi :
Proteomic Profiling of Ganglioside-Associated Microdomain in Malignant Melanomas,
HUPO 12th Annual World Congress, Yokohama, Japan, Sep. 2013. 橋本登 :
シアル酸結合レクチンSiglec7を介した癌の悪性形質増強と免疫監視逃避機構の解析,
第45回日本分子生物学会年会, 2022年12月. 沖若奈, 加納史也, 西原嵩晃, 橋本登, 山本朗仁 :
放射線唾液腺障害に対する歯髄幹細胞由来上清の治療効果の検討,
第64回歯科基礎医学会学術大会, 2022年9月.

(キーワード): 歯髄幹細胞 / 放射線性口腔乾燥 / 培養上清

猿山善章, 森岡莉彩, 加納史也, 橋本登, 山本朗仁 :
分泌型シアル酸認識レクチンを用いた関節リウマチの新規治療法の開発,
第76回NPO法人日本口腔科学会学術集会, 2022年4月.

(キーワード): シアル酸認識レクチン / 関節リウマチ

沖若奈, 加納史也, 西原嵩晃, 橋本登, 山本朗仁 :
⻭髄幹細胞培養上清の抗酸化効果による放射線性⼝腔乾燥症の治療メカニズム,
第76回NPO法人日本口腔科学会学術集会, 2022年4月.

(キーワード): 歯髄幹細胞 / 培養上清 / 口腔乾燥

森岡莉彩, 猿山善章, 加納史也, 橋本登, 山本朗仁 :
分泌型シアル酸認識レクチン-9とケモカインMCP-1 を用いた関節リウマチの新規治療法の開発,
四国歯学会第59回例会, 2022年3月.

(キーワード): シアル酸認識レクチン-9 / MCP-1 / 関節リウマチ

LINZE XIA, Fumiya Kano, Noboru Hashimoto and Akihito Yamamoto :
Conditioned Medium from the Stem Cells of Human Exfoliated Deciduous Teeth Ameliorates Experimental Temporomandibular Joint Osteoarthritis by Inducing M2 Phenotype of Macrophages,
蔵本免疫懇話会, Nov. 2021.

(キーワード): 培養上清 / 脱落乳歯歯髄幹細胞 / 変形性顎関節症 / M2マクロファージ

加納史也, LIU YAO, 橋本登, 松香芳三, 田中栄二, 山本朗仁 :
⻭髄幹細胞由来無⾎清培養上清は坐⾻神経結紮モデルマウスの神経障害性疼痛を改善する,
第63回歯科基礎医学会学術大会, 2021年9月.

(キーワード): 歯髄幹細胞 / 培養上清 / 神経障害性疼痛

西原嵩晃, 沖若奈, 加納史也, 橋本登, 河原林啓太, 山本朗仁 :
放射線唾液腺障害に対する歯髄幹細胞由来上清の治療効果の検討,
四国歯学会第57回例会, 2021年3月.

(キーワード): 歯髄幹細胞 / 培養上清 / 口腔乾燥

夏霖泽, 加納史也, 橋本登, 小笠原直子, LIU YAO, 田中栄二, 山本朗仁 :
:Analysis of the Therapeutic Mechanisms of SHED-CM for Experimentally Induced Temporomandibular Joint Osteoarthritis in Mice.,
四国歯学会雑誌, 2021年3月. 加納史也, 小笠原直子, 橋本登, 森浩喜, 宮嵜彩, 岩本勉, 田中栄二, 山本朗仁 :
歯髄幹細胞由来無血清培養上清を用いた変形性顎関節症の治療法開発,
第62回歯科基礎医学会学術大会, 2020年9月.

(キーワード): 変形性顎関節症 / 乳歯歯髄幹細胞 / 乳歯歯髄幹細胞由来培養上清

橋本登, 加納史也, 河原林啓太, LIU YAO, 夏霖泽, 山本朗仁 :
ヒト乳歯歯髄幹細胞由来培養液における皮膚炎モデルマウス治療効果因子のプロテオーム解析,
第41回日本炎症・再生医学会, 2020年7月. 加納史也, LIU YAO, 橋本登, 松香芳三, 田中栄二, 山本朗仁 :
歯髄幹細胞由来無血清培養上清は坐骨神経結紮モデルマウスの神経障害性疼痛を改善する,
日本炎症・再生医学会, 2020年7月. 橋本登, 加納史也, 河原林啓太, LIU YAO, 山本朗仁 :
ヒト乳歯歯髄幹細胞由来培養液における皮膚炎モデルマウス治療効果因子のプロテオーム解析,
第19回日本再生医療学会総会, 2020年5月. 加納史也, 小笠原直子, 橋本登, 森浩喜, 宮嵜彩, 岩本勉, 田中栄二, 山本朗仁 :
歯髄幹細胞由来無血清培養上清を用いた変形性顎関節症の治療法開発,
第19回日本再生医療学会, 20, 2020年3月. 後野秀一朗, 加納史也, 有馬秀貴, 橋本登, 寺町順平, 岩本勉, 山本朗仁 :
歯髄幹細胞由来無血清培養上清を用いた脊髄損傷の治療法開発,
徳島県歯科医学大会, 37, 2020年2月. 有馬秀貴, 加納史也, 後野秀一朗, 橋本登, 寺町順平, 岩本勉, 山本朗仁 :
間葉系幹細胞由来分泌因子がSchwann細胞の活性化に与える影響,
徳島県歯科医学大会, 36, 2020年2月. 河原林啓太, 加納史也, 橋本登, 寺町順平, 青田桂子, 東雅之, 岩本勉, 山本朗仁 :
歯髄幹細胞由来無血清培養上清を用いた口腔乾燥症の治療法の開発,
徳島県歯科医学大会, 20, 2020年2月. 小笠原直子, 加納史也, 橋本登, LIU YAO, 森浩喜, 寺町順平, 岩本勉, 田中栄二, 山本朗仁 :
歯髄幹細胞由来無血清培養上清を用いた変形性顎関節症の治療法開発,
徳島県歯科医学大会, 20, 2020年2月. 小笠原直子, 橋本登, 山本朗仁, 田中栄二 :
変形性顎関節症に対するヒト脱落乳歯歯髄幹細胞由来無血清馴化培地の治療効果,
第78回日本矯正歯科学会学術大会: 日本矯正歯科学会大会プログラム・抄録集 78回 Page183.(2019), 183, 2019年11月. 橋本登, 伊藤静香, 土田明子, H.Buiyan Robiul, 岡島徹也, 山本朗仁, 古川圭子, 大海雄介, 古川鋼一 :
シアル酸結合レクチン Siglec7 のガングリオシド GD3 認識に対するセラミド構造の影響,
38, 2019年8月. YAO RIU, 橋本登, 寺町順平, 松香芳三, 田中栄二, 山本朗仁 :
乳歯歯髄幹細胞培養上清によるマウス坐骨神経結紮モデルにおける神経障害性疼痛の改善．,
第40回日本炎症・再生医学会, 2019年7月.

研究会・報告書

加納史也, 橋本登, 山本朗仁 :
⻭髄幹細胞培養上清の抗酸化効果による放射線性⼝腔乾燥症の治療メカニズム,
四国免疫フォーラム, 2023年6月.

(キーワード): 歯髄幹細胞 / 放射線性口腔乾燥症 / 培養上清

特許: 山本朗仁, 加納史也, 橋本登, 高橋伸典 : 骨疾患を処置または予防するための組成物, 特願P275144 (2021年9月), .
作品: 研究者総覧に該当データはありませんでした。
補助金・競争的資金: 可溶性レクチンを用いた関節リウマチ病態制御機構の検討 (研究課題/領域番号: 23K06414 )
分泌型シアル酸認識レクチンによる関節再生メカニズムの解析 (研究課題/領域番号: 21H03055 )
乳歯歯髄幹細胞培養上清由来因子を用いた新規皮膚炎治療法の検討 (研究課題/領域番号: 20K08690 )
分泌型Siglec-9とMCP-1による単球系細胞の炎症組織再生型移行機構の解明 (研究課題/領域番号: 17K15720 )
シグレックとシアル酸含有糖鎖が生成する自然免疫チェックポイントの機構解明 (研究課題/領域番号: 15K15080 )
Siglec-7と認識糖鎖の結合による癌の悪性形質増強と免疫監視逃避機構の解析 (研究課題/領域番号: 26860320 )
研究者番号（90712365）による検索

その他: 研究者総覧に該当データはありませんでした。

研究者総覧で最新データを確認する

2024年5月17日更新

専門分野・研究分野: 糖鎖生物学 (Glycobiology)
所属学会・所属協会: 日本糖質学会
日本再生医療学会
委員歴・役員歴: 研究者総覧に該当データはありませんでした。
受賞: 研究者総覧に該当データはありませんでした。
活動: 研究者総覧に該当データはありませんでした。

Ｊグローバルで最新データを確認する

更新

2024年5月18日更新

Ｊグローバル

Jグローバル最終確認日: 2024/5/18 01:28
氏名（漢字）: 橋本登
氏名（フリガナ）: ハシモトノボル
氏名（英字）: Hashimoto Noboru
所属機関: JグローバルAPIで取得できませんでした。

リサーチマップ

researchmap最終確認日: リサーチマップAPIで取得できませんでした。
氏名（漢字）: リサーチマップAPIで取得できませんでした。
氏名（フリガナ）: リサーチマップAPIで取得できませんでした。
氏名（英字）: リサーチマップAPIで取得できませんでした。
プロフィール: リサーチマップAPIで取得できませんでした。
登録日時: リサーチマップAPIで取得できませんでした。
更新日時: リサーチマップAPIで取得できませんでした。
アバター画像URI: リサーチマップAPIで取得できませんでした。
ハンドル: リサーチマップAPIで取得できませんでした。
eメール: リサーチマップAPIで取得できませんでした。
eメール（その他）: リサーチマップAPIで取得できませんでした。
携帯メール: リサーチマップAPIで取得できませんでした。
性別: リサーチマップAPIで取得できませんでした。
没年月日: リサーチマップAPIで取得できませんでした。
所属ID: リサーチマップAPIで取得できませんでした。
所属: リサーチマップAPIで取得できませんでした。
部署: リサーチマップAPIで取得できませんでした。
職名: リサーチマップAPIで取得できませんでした。
学位: リサーチマップAPIで取得できませんでした。
学位授与機関: リサーチマップAPIで取得できませんでした。
URL: リサーチマップAPIで取得できませんでした。
科研費研究者番号: リサーチマップAPIで取得できませんでした。
Google Analytics ID: リサーチマップAPIで取得できませんでした。
ORCID ID: リサーチマップAPIで取得できませんでした。
その他の所属ID: リサーチマップAPIで取得できませんでした。
その他の所属名: リサーチマップAPIで取得できませんでした。
その他の所属部署: リサーチマップAPIで取得できませんでした。
その他の所属職名: リサーチマップAPIで取得できませんでした。
最近のエントリー: リサーチマップAPIで取得できませんでした。
Read会員ID: リサーチマップAPIで取得できませんでした。
経歴: リサーチマップAPIで取得できませんでした。
受賞: リサーチマップAPIで取得できませんでした。
Misc: リサーチマップAPIで取得できませんでした。
論文: リサーチマップAPIで取得できませんでした。
講演・口頭発表等: リサーチマップAPIで取得できませんでした。
書籍等出版物: リサーチマップAPIで取得できませんでした。
研究キーワード: リサーチマップAPIで取得できませんでした。
研究分野: リサーチマップAPIで取得できませんでした。
所属学協会: リサーチマップAPIで取得できませんでした。
担当経験のある科目: リサーチマップAPIで取得できませんでした。
その他: リサーチマップAPIで取得できませんでした。
Works: リサーチマップAPIで取得できませんでした。
特許: リサーチマップAPIで取得できませんでした。
学歴: リサーチマップAPIで取得できませんでした。
委員歴: リサーチマップAPIで取得できませんでした。
社会貢献活動: リサーチマップAPIで取得できませんでした。

ＫＡＫＥＮで最新データを確認する

2024年5月18日更新

研究者番号: 90712365

所属（現在）: 2024/4/1 : 徳島大学, 大学院医歯薬学研究部(歯学域), 助教

所属（過去の研究課題 情報に基づく）*注記: 2018/4/1 – 2023/4/1 : 徳島大学, 大学院医歯薬学研究部(歯学域), 助教
2017/4/1 : 徳島大学, 大学院医歯薬学研究部(歯学系), 助教
2016/4/1 : 名古屋大学, 医学系研究科, 研究員
2015/4/1 : 名古屋大学, 医学(系)研究科(研究院), 研究機関研究員
2014/4/1 – 2015/4/1 : 名古屋大学, 医学(系)研究科(研究院), 研究員

審査区分/研究分野

研究代表者

生物系 / 医歯薬学 / 基礎医学 / 免疫学
小区分53050:皮膚科学関連
小区分49010:病態医化学関連

研究代表者以外

生物系 / 医歯薬学 / 基礎医学 / 病態医化学
小区分56020:整形外科学関連

キーワード

研究代表者

糖鎖 / 癌 / 免疫 / 免疫監視機構 / 質量分析 / シアル酸 / Siglec-9 / 炎症 / 組織修復 / マクロファージ / 抗炎症 / 組織再生機構 / 炎症制御 / 組織再生 / 炎症性皮膚疾患 / Atopic dermatitis / 乳歯歯髄幹細胞培養上清 / CD4+T細胞 / 乾癬 / 皮膚バリア / 皮膚炎 / 可溶性レクチン / 関節リウマチ / 破骨細胞 / 滑膜線維芽細胞

研究代表者以外

シグレック / 自然免疫 / シアル酸 / チェックポイント / 癌免疫 / 糖鎖 / 細胞傷害 / 糖脂質 / シグナル / 単球 / マクロファージ / アストロサイトーマ / シアル酸認識レクチン / 関節リウマチ / Siglec9 / M2マクロファージ / 軟骨細胞 / 破骨細胞 / 関節炎 / 分泌型シアル酸認識レクチン / 関節再生

研究課題研究成果共同研究者

「研究課題をさがす」で表示
テキスト（CSV）で出力

テキスト（CSV）で出力

注目研究はありません。

研究者を探す

橋本 登

Ｊグローバル

リサーチマップ

研究代表者

研究代表者以外

研究代表者

研究代表者以外

橋本登