Updated on 2025/01/20

写真a

 
MATSUDA Yasuyuki
 
Organization
School of Medicine Medical Course Basic Medicine Microbiology and Immunochemistry
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Degree

  • 博士（理学） ( 九州大学 )

  • 修士（理学） ( 九州大学 )

  • 学士（理学） ( 九州大学 )

Research Interests

  • 細菌学

  • 自然免疫

Research Areas

  • Life Science / Cell biology

  • Life Science / Molecular biology

  • Life Science / Medical biochemistry

  • Life Science / Functional biochemistry

Education

  • Kyushu University   Graduate School of Sciences   Department of Biology

    2005.4 - 2008.3

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  • Kyushu University   Graduate School of Sciences   Department of Biology

    2003.4 - 2005.3

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  • Kyushu University   School of Sciences   Department of Biology

    1999.4 - 2003.3

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Research History

  • Asahikawa Medical College   Assistant Professor

    2013.4

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  • Asahikawa Medical College

    2011.7 - 2013.3

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  • 日本学術振興会   特別研究員PD

    2009.4 - 2011.6

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  • 国立循環器病センター研究所   病因部   流動研究員

    2008.4 - 2009.3

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Professional Memberships

Studying abroad experiences

  • 2007.1 - 2007.3   Department of Comparative Physiology, Evolutionary Biology Centre, Uppsala University   Swedish Foundation for International cooperation in research and higher education

Papers

  • Three pentraxins C-reactive protein, serum amyloid p component and pentraxin 3 mediate complement activation using Collectin CL-P1. Reviewed International journal

    Nitai Roy, Katsuki Ohtani, Yoshihiko Hidaka, Yoshiro Amano, Yasuyuki Matsuda, Kenichiro Mori, Insu Hwang, Norimitsu Inoue, Nobutaka Wakamiya

    Biochimica et biophysica acta. General subjects   1861 ( 2 )   1 - 14   2017.2

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    Language：English   Publishing type：Research paper (scientific journal)  

    BACKGROUND: Pentraxins (PTXs) are a superfamily of multifunctional conserved proteins involved in acute-phase responses. Recently, we have shown that collectin placenta 1 (CL-P1) and C-reactive protein (CRP) mediated complement activation and failed to form terminal complement complex (TCC) in normal serum conditions because of complement factor H inhibition. METHODS: We used CL-P1 expressing CHO/ldlA7 cells to study the interaction with PTXs. Soluble type CL-P1 was used in an ELISA assay for the binding, C3 and TCC deposition experiments. Furthermore, we used our previously established CL-P1 expressing HEK293 cells for the C3 fragment and TCC deposition assay. RESULTS: We demonstrated that CL-P1 also bound serum amyloid p component (SAP) and pentraxin 3 (PTX3) to activate the classical pathway and the alternative pathway using factor B. CRP and PTX3 further amplified complement deposition by properdin. We found that CRP and PTX3 recruit CFH, whereas SAP recruits C4 binding protein on CL-P1 expressing cell surfaces to prevent the formation of TCC in normal serum conditions. In addition, depletion of CFH, C4BP and complement factor I (CFI) failed to prevent TCC formation both in ELISA and cell experiments. Furthermore, soluble complement receptor 1, an inhibitor of all complement pathways prevents PTX induced TCC formation. CONCLUSION: Our current study hypothesizes that the interaction of pentraxins with CL-P1 is involved in complement activation. GENERAL SIGNIFICANCE: CL-P1 might generally inhibit PTX induced complement activation and host damage to protect self-tissues.

    DOI： 10.1016/j.bbagen.2016.11.023

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  • Plasminogen Tochigi mice exhibit phenotypes similar to wild-type mice under experimental thrombotic conditions. Reviewed International journal

    Yuko Tashima, Fumiaki Banno, Toshiyuki Kita, Yasuyuki Matsuda, Hiroji Yanamoto, Toshiyuki Miyata

    PloS one   12 ( 7 )   e0180981   2017

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    Plasminogen (Plg) is a precursor of plasmin that degrades fibrin. A race-specific A620T mutation in Plg, also known as Plg-Tochigi, originally identified in a patient with recurrent venous thromboembolism, causes dysplasminogenemia with reduced plasmin activity. The Plg-A620T mutation is present in 3-4% of individuals in East Asian populations, and as many as 50,000 Japanese are estimated to be homozygous for the mutant 620T allele. In the present study, to understand the changes of thrombotic phenotypes in individuals with the mutant 620T allele, we generated knock-in mice carrying the homozygous Plg-A622T mutation (PlgT/T), an equivalent to the A620T mutation in human Plg. PlgT/T mice grew normally but showed severely reduced plasmin activity activated by urokinase, equivalent to ~8% of that in wild-type mice. In vitro fibrin clot lysis in plasma was significantly slower in PlgT/T mice than in wild-type mice. However, all experimental models of electrolytic deep vein thrombosis, tissue factor-induced pulmonary embolism, transient focal brain ischaemic stroke, or skin-wound healing showed largely similar phenotypes between PlgT/T mice and wild-type mice. Protein S-K196E mutation (Pros1E/E) is a race-specific genetic risk factor for venous thromboembolism. Coexistence in mice of PlgT/T and Pros1E/E did not affect pulmonary embolism symptoms, compared with those in Pros1E/E mice. Hence, the present study showed that the Plg-A622T mutation, which confers ~8% plasmin activity, does not increase the risk of thrombotic diseases in mice under experimental thrombotic conditions and does not modify the thrombotic phenotype observed in Pros1E/E mice. PlgT/T mice can be used to investigate the potential pathophysiological impact of the Plg-A620T mutation.

    DOI： 10.1371/journal.pone.0180981

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  • Collectin Kidney 1 Plays an Important Role in Innate Immunity against Streptococcus pneumoniae Infection. Reviewed International journal

    Insu Hwang, Kenichiro Mori, Katsuki Ohtani, Yasuyuki Matsuda, Nitai Roy, YounUck Kim, Yasuhiko Suzuki, Nobutaka Wakamiya

    Journal of innate immunity   9 ( 2 )   217 - 228   2017

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    Language：English   Publishing type：Research paper (scientific journal)  

    Collectins are C-type lectins that are involved in innate immunity as pattern recognition molecules. Recently, collectin kidney 1 (CL-K1) has been discovered, and in vitro studies have shown that CL-K1 binds to microbes and activates the lectin complement pathway. However, in vivo functions of CL-K1 against microbes have not been elucidated. To investigate the biological functions of CL-K1, we generated CL-K1 knockout (CL-K1-/-) mice and then performed a Streptococcus pneumoniae infection analysis. First, we found that recombinant human CL-K1 bound to S. pneumoniae in a calcium-dependent manner, and induced complement activation. CL-K1-/- mice sera formed less C3 deposition on S. pneumoniae. Furthermore, immunofluorescence analysis in the wild-type (WT) mice demonstrated that CL-K1 and C3 were localized on S. pneumoniae in infected lungs. CL-K1-/- mice revealed decreased phagocytosis of S. pneumoniae. Consequently, less S. pneumoniae clearance was observed in their lungs. CL-K1-/- mice showed severe pulmonary inflammation and weight loss in comparison with WT mice. Finally, the decreased clearance and severe pulmonary inflammation caused by S. pneumoniae infection might cause higher CL-K1-/- mice lethality. Our results suggest that CL-K1 might play an important role in host protection against S. pneumoniae infection through the activation of the lectin complement pathway.

    DOI： 10.1159/000453316

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  • Collectin CL-P1 utilizes C-reactive protein for complement activation. Reviewed International journal

    Nitai Roy, Katsuki Ohtani, Yasuyuki Matsuda, Kenichiro Mori, Insu Hwang, Yasuhiko Suzuki, Norimitsu Inoue, Nobutaka Wakamiya

    Biochimica et biophysica acta   1860 ( 6 )   1118 - 28   2016.6

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    BACKGROUND: C-reactive protein (CRP) is a plasma pentraxin family protein that is massively induced as part of the innate immune response to infection and tissue injury. CRP and other pentraxin proteins can activate a complement pathway through C1q, collectins, or on microbe surfaces. It has been found that a lectin-like oxidized LDL receptor 1 (LOX-1), which is an endothelial scavenger receptor (SR) having a C-type lectin-like domain, interacts with CRP to activate the complement pathway using C1q. However it remains elusive whether other lectins or SRs are involved in CRP-mediated complement activation and the downstream effect of the complement activation is also unknown. METHODS: We prepared CHO/ldlA7 cells expressing collectin placenta-1 (CL-P1) and studied the interaction of CRP with cells. We further used ELISA for testing binding between proteins. We tested for C3 fragment deposition and terminal complement complex (TCC) formation on HEK293 cells expressing CL-P1. RESULTS: Here, we demonstrated that CL-P1 bound CRP in a charge dependent manner and the interaction of CRP with CL-P1 mediated a classical complement activation pathway through C1q and additionally drove an amplification pathway using properdin. However, CRP also recruits complement factor H (CFH) on CL-P1 expressing cell surfaces, to inhibit the formation of a terminal complement complex in normal complement serum conditions. GENERAL SIGNIFICANCE: The interaction of collectin CL-P1 with CFH might be key for preventing attack on "self" as a result of complement activation induced by the CL-P1 and CRP interaction.

    DOI： 10.1016/j.bbagen.2016.02.012

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  • Scavenger receptor CL-P1 mainly utilizes a collagen-like domain to uptake microbes and modified LDL. Reviewed International journal

    Kenichiro Mori, Katsuki Ohtani, Jang Seonjae, Kim YonuUck, Hwang Insu, Nitai Roy, Yasuyuki Matsuda, Suzuki Yasuhiko, Nobutaka Wakamiya

    Biochimica et Biophysica Acta (BBA) - General Subjects   1840 ( 12 )   3345 - 3356   2014.12

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    DOI： 10.1016/j.bbagen.2014.08.015

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  • Peptidoglycan activation of the proPO-system without a peptidoglycan receptor protein (PGRP)? Reviewed International journal

    Haipeng Liu, Chenglin Wu, Yasuyuki Matsuda, Shun-Ichiro Kawabata, Bok Luel Lee, Kenneth Söderhäll, Irene Söderhäll

    Developmental and comparative immunology   35 ( 1 )   51 - 61   2011.1

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    Recognition of microbial polysaccharide by pattern recognition receptors triggers the prophenoloxidase (proPO) cascade, resulting in melanin synthesis and its deposition on the surface of invading pathogens. Several masquerade-like proteins and serine proteinase homologues have been shown to be involved in the proPO activation in insects. In this study, a novel serine proteinase homologue, Pl-SPH2, was found and isolated as a 30kDa protein from hemocytes of the freshwater crayfish, Pacifastacus leniusculus, by its binding property to a partially lysozyme digested or TCA-treated insoluble Lysine (Lys)-type peptidoglycan (PGN) and soluble polymeric Lys-type PGN. Two other proteins, the Pl-SPH1 and lipopolysaccharide- and β-1,3-glucan-binding protein (LGBP) were also found in the several different PGN-binding assays. However no PGRP homologue was detected. Neither was any putative PGRP found after searching available crustacean sequence databases. If RNA interference of Pl-SPH2, Pl-SPH1 or LGBP in the crayfish hematopoietic tissue cell culture was performed, it resulted in lower PO activity following activation of the proPO-system by soluble Lys-type PGN. Taken together, we report for the first time that Lys-type PGN is a trigger of proPO-system activation in a crustacean and that two Pl-SPHs are involved in this activation possibly by forming a complex with LGBP and without a PGRP.

    DOI： 10.1016/j.dci.2010.08.005

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  • Exploration of molecules involved in control of platelet integrin αIIbβ3 function using a random mutagenesis approach Reviewed

    Shigenori Honda, Hiroko Shirotani-Ikejima, Yasuyuki Matsuda, Seiji Tadokoro, Yusuke Maeda, Taroh Kinoshita, Yoshiaki Tomiyama, Toshiyuki Miyata

    Jpn. J. Thromb. Hemost.   20 ( 6 )   615 - 621   2009.12

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    Language：Japanese   Publisher：The Japanese Society on Thrombosis and Hemostasis  

    DOI： 10.2491/jjsth.20.615

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  • An arthropod cuticular chitin-binding protein endows injured sites with transglutaminase-dependent mesh. Reviewed International journal

    Yasuyuki Matsuda, Takumi Koshiba, Tsukasa Osaki, Haruka Suyama, Fumio Arisaka, Yoshihiro Toh, Shun-Ichiro Kawabata

    The Journal of biological chemistry   282 ( 52 )   37316 - 24   2007.12

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    In mammals, the cornified cell envelope forms beneath the plasma membrane in epithelia and provides a vital physical barrier consisting of insoluble proteins cross-linked by transglutaminase (TGase). In the horseshoe crab Tachypleus tridentatus, TGase is stored in hemocytes and secreted in response to the simulation of bacterial lipopolysaccharides. Here we characterized a TGase substrate designated as caraxin that was identified in horseshoe crab cuticle. One of the homologs, caraxin-1, possessed a unique domain structure consisting of N-and C-terminal heptad repeats and a central domain with a tandem-repeated structure of a pentapeptide. Western blotting showed the specific localization of caraxin-1 in sub-cuticular epidermis. Moreover, we identified the pentapeptide motif to be a chitin-binding unit. Analytical ultracentrifugation revealed that caraxin-1 exists as an oligomer with 310-350 kDa, which is approximately 20-mer based on the molecular mass of the monomer. The oligomers were cross-linked by TGase to form an elaborate mesh with honeycomb structures, which was electron-microscopically found to be different from the clotting mesh triggered by lipopolysaccharide-induced hemocyte exocytosis. We determined several cross-linking sites in the N-and C-terminal domains of caraxin-1. The replacements of Leu to Pro at positions 36 and 118 in caraxin-1 reduced the alpha-helix content, which destroyed the TGase-dependent mesh, thus indicating the importance of the N-and C-terminal domains for the proper mesh formation. In arthropods, TGase-dependent protein cross-linking may be involved in the initial stage of host defense at the sub-cuticular epidermis, as in the case of mammalian skin.

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  • A cysteine-rich protein from an arthropod stabilizes clotting mesh and immobilizes bacteria at injury sites. Reviewed International journal

    Yasuyuki Matsuda, Tsukasa Osaki, Tomoyuki Hashii, Takumi Koshiba, Shun-ichiro Kawabata

    The Journal of biological chemistry   282 ( 46 )   33545 - 52   2007.11

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    Hemolymph coagulation in arthropods plays key roles in host defense, including sealing wounds to staunch bleeding and immobilizing invading microorganisms. We have previously reported that horseshoe crab transglutaminase (TGase) promotes cross-linking of a clotting protein (coagulin) with hemocyte-derived proteins (proxins), resulting in the formation of stable coagulin fibrils. Here we show that TGase also cross-links proxins to another hemocyte-derived protein named stablin. Stablin is a cysteine-rich protein of 131 residues. Surface plasmon resonance analysis revealed the specific interaction of stablin with proxin-1 at K(d) = 4.0 x 10(-9) m. Stablin was predominantly localized in the large granules of hemocytes and secreted by lipopolysaccharide-induced exocytosis. Interestingly, stablin bound to chitin at K(d) = 1.5 x 10(-8) m, as determined by using a quartz-crystal microbalance. Stablin also interacted with lipopolysaccharides and lipoteichoic acids and exhibited bacterial agglutinating activity against Gram-positive and -negative bacteria. Immunostaining showed that stablin is co-localized with coagulin in the clotting fibrils that effectively trap bacteria. Moreover, an anti-stablin antibody strongly inhibited the proper formation of the clotting fibrils. These data suggest that stablin promotes the formation of the clotting mesh and the immobilization of invading microbes at injury sites. In arthropods, the TGase-mediated cross-linking may play an important role in the initial stage of host defense, wound closure, and healing, as in the case of mammals.

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  • Comprehensive sequence analysis of horseshoe crab cuticular proteins and their involvement in transglutaminase-dependent cross-linking Reviewed International journal

    IIJIMA Manabu, HASHIMOTO Tomonori, MATSUDA Yasuyuki, NAGAI Taku, YAMANO Yuichiro, ICHI Tomohiko, OSAKI Tsukasa, KAWABATA Shun-ichiro

    FEBS Journal   272 ( 18 )   4774 - 86   2005

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    Arthropod cuticles play an important role as the first barrier against invading pathogens. We extensively determined the sequences of horseshoe crab cuticular proteins. Proteins extracted from a part of the ventral side of the cuticle were purified by chitin-affinity chromatography, and separated by two-dimensional SDS/PAGE. Proteins appearing on the gel were designated high molecular mass chitin-binding proteins, and these proteins were then grouped into classes based on their approximate isoelectric points and predominant amino acid compositions. Members of groups designated basic G, basic Y, and acidic S groups contained a so-called Rebers and Riddiford consensus found in arthropod cuticular proteins. Proteins designated acidic DE25 and DE29 each contained a Cys-rich domain with sequences similar to those of insect peritrophic matrix proteins and chitinases. In contrast, basic QH4 and QH10 contained no consensus sequences found in known chitin-binding proteins. Alternatively, a low molecular mass chitin-binding fraction was prepared by size exclusion chromatography, and 15 low molecular mass chitin-binding proteins, named P1 through P15, were isolated. With the exception of P9 and P15, all were found to be identical to known antimicrobial peptides. P9 consisted of a Kunitz-type chymotrypsin inhibitor sequence, and P15 contained a Cys-rich motif found in insulin-like growth factor-binding proteins. Interestingly, we observed transglutaminase-dependent polymerization of nearly all high molecular mass chitin-binding proteins, a finding suggests that transglutaminase-dependent cross-linking plays an important role in host defense in the arthropod cuticle, analogous to that observed in the epidermal cornified cell envelope in mammals.

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MISC

  • 膜コレクチンCL-P1はPentraxinを利用して補体系を活性化する

    Nitai Roy, 大谷 克城, 日高 義彦, 天野 芳郎, 松田 泰幸, 森 健一郎, 黄 仁秀, 井上 徳光, 若宮 伸隆

    北海道医学雑誌   92 ( 1 )   30 - 30   2017.5

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  • コレクチンCL-P1はPentraxinを介して補体系を活性化する

    ROY Nitai, 大谷克城, 日高義彦, 天野芳郎, 松田泰幸, 森健一郎, HWANG Insu, 井上徳光, 若宮伸隆

    日本糖質学会年会要旨集   36th   2017

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  • スカベンジャー受容体CL-P1は,Pentraxinを介して補体系を活性化する

    ROY Nitai, 大谷克城, 日高義彦, 天野芳郎, 松田泰幸, 森健一郎, HWANG Insu, 井上徳光, 若宮伸隆

    補体   54 ( 1 )   33 - 34   2017

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    Language：Japanese   Publisher：(一社)日本補体学会  

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  • コレクチンCL-LKはDNAに結合して補体系を活性化する

    松田泰幸, 大谷克城, ニタイ ロイ, 森健一郎, 黄仁秀, 若宮伸隆

    日本生化学会大会(Web)   90th   [1LBA - 005]   2017

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    Language：Japanese   Publisher：生命科学系学会合同年次大会運営事務局  

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  • Collectin CL-P1 is involved in C-reactive protein-mediated complement activation

    Nitai Roy, Katsuki Ohtani, Yasuyuki Matsuda, Kenichiro Mori, Insu Hwang, Yasuhiko Suzuki, Norimitsu Inoue, Nobutaka Wakamiya

    IMMUNOBIOLOGY   221 ( 10 )   1215 - 1215   2016.10

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    Language：English   Publishing type：Research paper, summary (international conference)   Publisher：ELSEVIER GMBH, URBAN & FISCHER VERLAG  

    DOI： 10.1016/j.imbio.2016.06.201

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  • In vitro and in vivo roles in Collectin Kidney 1 (CL-K1) with innate immunity against Streptococcus pneumoniae

    Insu Hwang, Kenichiro Mori, Katsuki Ohtani, Yasuyuki Matsuda, Nitai Roy, YounUck Kim, Nobutaka Wakamiya

    IMMUNOBIOLOGY   221 ( 10 )   1217 - 1217   2016.10

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    Language：English   Publishing type：Research paper, summary (international conference)   Publisher：ELSEVIER GMBH, URBAN & FISCHER VERLAG  

    DOI： 10.1016/j.imbio.2016.06.205

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  • Structural characterization of novel collectins, CL-K1, CL-L1, and CL-LK in blood

    Yasuyuki Matsuda, Katsuki Ohtani, Nitai Roy, Insu Hwang, Kenichiro Mori, Nobutaka Wakamiya

    IMMUNOBIOLOGY   221 ( 10 )   1215 - 1215   2016.10

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    Language：English   Publishing type：Research paper, summary (international conference)   Publisher：ELSEVIER GMBH, URBAN & FISCHER VERLAG  

    DOI： 10.1016/j.imbio.2016.06.202

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  • 新規コレクチンCL-K1は、マウスにおける肺炎球菌感染に対して防御的に働く

    黄 仁秀, 森 健一郎, 大谷 克城, 松田 泰幸, ロイ・ニタイ, 若宮 伸隆

    日本生化学会大会プログラム・講演要旨集   89回   [3T07 - 06(3P   2016.9

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  • 膜型コレクチンCL-P1は、CRPを介して補体経路を活性化する

    Roy Nitai, 大谷 克城, 松田 泰幸, 森 健一郎, 黄 仁秀, 井上 徳光, 若宮 伸隆

    日本生化学会大会プログラム・講演要旨集   89回   [3T07 - 05(3P   2016.9

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  • コレクチンCL-P1は,急性期タンパクCRPを介して補体経路を活性化する

    大谷克城, ROY Nitai, 松田泰幸, 森健一郎, HWANG Insu, 井上徳光, 若宮伸隆

    日本糖質学会年会要旨集   35th   2016

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  • 新規コレクチンCL-K1は,マウスにおける肺炎球菌感染に対して防御的に働く

    黄仁秀, 森健一郎, 大谷克城, 松田泰幸, ロイ ニタイ, 若宮伸隆

    日本生化学会大会(Web)   89th   [3T07 - 057)]   2016

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  • 膜型コレクチンCL-P1は,CRPを介して補体経路を活性化する

    ROY Nitai, 大谷克城, 松田泰幸, 森健一郎, 黄仁秀, 井上徳光, 若宮伸隆

    日本生化学会大会(Web)   89th   [3T07 - 054)]   2016

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  • コレクチンCL-L1の分子構造と組織局在に関する解析

    松田泰幸

    旭川医科大学研究フォーラム   15 ( 1 )   65 - 66   2015

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    Language：Japanese   Publisher：旭川医科大学  

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    Other Link： http://search.jamas.or.jp/link/ui/2015361852

  • CL-K1は,肺炎球菌感染に対し,補体レクチン経路を介して生体防御に機能する

    HWANG Insu, 森健一郎, 松田泰幸, ROY Nitai, 大谷克城, 若宮伸隆

    日本糖質学会年会要旨集   34th   2015

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  • 新規コレクチンCL-K1と相互作用する血漿由来タンパク質の同定

    松田泰幸, 大谷克城, 森健一郎, ROY Nitai, HWANG Insu, 若宮伸隆

    日本糖質学会年会要旨集   34th   2015

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  • 新規コレクチンCL-K1の糖鎖認識と生物学的活性についての解析

    大谷克城, GIRIJA Umakhanth Venkatraman, 森健一郎, 吉崎隆之, 松田泰幸, HWANG Insu, ROY Nitai, WALLIS Russell, 若宮伸隆

    日本糖質学会年会要旨集   34th   2015

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  • コレクチンCL-K1の糖鎖認識と3MC症候群における変異の分子機構への影響

    大谷克城, GIRIJA Umakhanth Venkatraman, 森健一郎, 吉崎隆之, 松田泰幸, 黄仁秀, ROY Nitani, WALLIS Russell, 若宮伸隆

    日本生化学会大会(Web)   88th   [2P0289] - [2P0289]   2015

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  • スカベンジャー受容体CL-P1は,CRPを介して古典的経路を活性化する

    ROY Nitai, 大谷克城, 松田泰幸, 森健一郎, HWANG Insu, 若宮伸隆

    補体   52 ( 1 )   46 - 46   2015

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  • コレクチンCL-K1の生化学的解析

    大谷克城, 森健一郎, HWANG Insu, 吉崎隆之, 松田泰幸, ROY Nitai, 若宮伸隆

    日本糖質学会年会要旨集   33rd   2014

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  • 日本人に高頻度に見られるプラスミノーゲン栃木変異をもつ遺伝子改変マウスの血栓傾向の解析

    田嶌優子, 坂野史明, 喜多俊行, 松田泰幸, 柳本広二, 宮田敏行

    日本病態プロテアーゼ学会学術集会プログラム抄録集   19th   2014

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  • コレクチンCL-K1の凝固系への関与について

    大谷克城, TAKAHASHI Kazue, 早川峰司, 森健一郎, 黄仁秀, 吉崎隆之, 松田泰幸, ニタイ ロイ, 丸藤哲, 若宮伸隆

    日本生化学会大会(Web)   87th   [2T16a - 02]   2014

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  • コレクチンCL-K1の生体防御機能に関する検討

    HWANG Insu, 森健一郎, 松田泰幸, ROY Nitai, 大谷克城, 若宮伸隆

    補体   51 ( 1 )   58 - 59   2014

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  • コレクチンCL-L1の組織局在と分子構造に関する解析

    松田泰幸, ROY Nitai, 森健一郎, HWANG Insu, 大谷克城, 若宮伸隆

    補体シンポジウム講演集   50th   2013

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  • マウスプラスミノーゲン栃木変異は血漿プラスミン活性を低下させるが血栓塞栓症の原因にはならない

    田嶌優子, 坂野史明, 喜多俊行, 松田泰幸, 柳本広二, 宮田敏行

    日本生化学会大会(Web)   86th   3P - 447   2013

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  • プラスミノーゲン栃木変異ホモ接合体マウスの血栓傾向の解析

    田嶌優子, 坂野史明, 喜多俊行, 松田泰幸, 柳本広二, 柳本広二, 宮田敏行

    日本血栓止血学会誌   24 ( 2 )   194 - 194   2013

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  • コレクチンCL-L1の組織局在と分子構造に関する解析

    松田泰幸, ROY Nitai, 森健一郎, HWANG Insu, 大谷克城, 若宮伸隆

    日本生化学会大会(Web)   86th   1T06p - 09   2013

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  • コレクチンCL-L1の組織局在と分子構造に関する解析

    松田泰幸, ROY Nitai, 森健一郎, HWANG Insu, 大谷克城, 若宮伸隆

    日本糖質学会年会要旨集   32nd   31 - 32   2013

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  • コレクチンCL-K1のマウスおよびヒト組織における発現検討

    大谷克城, 本村亘, 吉崎隆之, 森健一郎, 松田泰幸, HWANG Insu, CHANDRA Roy, 吉田逸朗, 鈴木定彦, 若宮伸隆

    日本糖質学会年会要旨集   31st   2012

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  • 組織におけるコレクチンCL-K1の生化学的検討

    大谷克城, 本村亘, 吉崎隆之, 森健一郎, 松田泰幸, HWANG Insu, ROY Nitai, 吉田逸朗, 鈴木定彦, 若宮伸隆

    日本生化学会大会(Web)   85th   3T16 - 07   2012

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  • コレクチンCL-K1の組織における発現検討

    大谷克城, 本村亘, 吉崎隆之, 森健一郎, 松田泰幸, HWANG Insu, ROY Nitai, 吉田逸朗, 鈴木定彦, 若宮伸隆

    補体シンポジウム講演集   49th   23 - 23   2012

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  • コレクチンCL-K1のヒト血中濃度

    大谷克城, 吉崎隆之, 森健一郎, 本村亘, 松田泰幸, HWANG Insu, 吉田逸朗, KIM YounUck, 鈴木定彦, 若宮伸隆

    補体シンポジウム講演集   48th   31 - 31   2011

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  • コレクチンCL-K1の機能とヒト血中濃度について

    大谷克城, 吉崎隆之, 森健一郎, 本村亘, 松田泰幸, HWANG Insu, 吉田逸朗, KIM Younuck, 鈴木定彦, 若宮伸隆

    日本分子生物学会年会プログラム・要旨集(Web)   34th   2011

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  • インテグリン活性化におけるintegrin-linked kinaseの役割

    本田繁則, 池島裕子, 松田泰幸, 田所誠司, 冨山佳昭, 冨山佳昭, 宮田敏行

    臨床血液   51 ( 9 )   1191 - 1191   2010

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  • 血栓の成長を促進するメカニズム 〜ずり応力変化の重要性〜

    松田泰幸

    蛋白質・核酸・酵素   54 ( 9 )   1408 - 1408   2009.9

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  • 抗原変異はRNAiによって制御されている

    松田泰幸

    蛋白質・核酸・酵素   54 ( 3 )   276 - 276   2009.3

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  • An arthropod cuticular chitin-binding protein endows injured sites with transglutaminase-dependent mesh

    松田泰幸, 小柴琢己, 尾崎司, 陶山晴香, 有坂文雄, 藤義博, 川畑俊一郎

    生化学   2007

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  • カブトガニ外皮タンパク質(カラキシン)は,トランスグルタミナーゼにより架橋され網目状繊維を形成する

    松田泰幸, 小柴琢己, 尾崎司, 有坂文雄, 川畑俊一郎

    日本蛋白質科学会年会プログラム・要旨集   7th   2007

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  • Characterization of a recombinant caraxin-1, a horseshoe crab cuticular protein for transglutaminase-dependent cross-linking

    MATSUDA Yasuyuki, OSAKI Tsukasa, KOSHIBA Takumi, KAWABATA Shun-ichiro

    生化学   77 ( 8 )   2005

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  • Cuticular chitin-binding proteins from horseshoe crab exoskeleton are involved in transglutaminase-dependent cross-linking

    IIJIMA Manabu, MATSUDA Yasuyuki, OSAKI Tsukasa, YOSHIDA Ryoko, KOSHIBA Takumi, KAWABATA Shun-ichiro

    生化学   77 ( 8 )   2005

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  • Characterization of a transglutaminase substrate identified from cuticular chitin-binding proteins in horseshoe crabs

    MATSUDA Y, OSAKI T, KAWABATA S

    生化学   76 ( 8 )   2004

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  • Cuticular Chitin-Binding Proteins in Horseshoe Crabs

    IIJIMA M, HASHIMOTO T, NAGAI T, YAMANO Y, MATSUDA Y, OSAKI T, KAWABATA S

    Trends in Glycoscience and Glycotechnology   16 ( Supplement )   2004

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  • The roles of horseshoe crab hemocyte transglutaminase in both hemolymph coagulation and innate immunity.

    OSAKI T, MATSUDA Y, HASHIMOTO T, IIJIMA M, KAWABATA S

    生化学   75 ( 8 )   2003

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Presentations

  • コレクチンCL-P1は、急性期タンパクCRPを介して補体経路を活性化する

    大谷克城, ロイ・ニタイ, 松田泰幸, 森健一郎, 黄仁秀, 井上徳光, 若宮伸隆

    第36回日本糖質学会年会  2017.7 

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    Event date： 2017.7

    Language：Japanese   Presentation type：Poster presentation  

    Venue：旭川  

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  • プラスミノーゲン栃木変異ホモ接合体マウスの血栓傾向の解析

    田嶌 優子, 坂野 史明, 喜多 俊行, 松田 泰幸, 柳本 広二, 宮田 敏行

    第35回日本血栓止血学会学術集会 

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    Event date： 2013.5 - 2013.6

    Venue：山形  

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  • 組織におけるコレクチンCL-K1の生化学的検討

    大谷克城, 本村亘, 吉崎隆之, 森健一郎, 松田泰幸, 黄仁秀, ロイ・ニタイ, 吉田逸朗, 鈴木定彦, 若宮伸隆

    第85回日本生化学会大会 

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    Event date： 2012.12

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：福岡  

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  • コレクチンCL-K1の機能とヒト血中濃度について

    大谷克城, 吉崎隆之, 森健一郎, 本村亘, 松田泰幸, 黄仁秀, 吉田逸朗, 金然旭, 鈴木定彦, 若宮伸隆

    第34回日本分子生物学会年会 

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    Event date： 2011.12

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：横浜  

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  • コレクチンCL-K1のヒト血中濃度

    大谷克城, 吉崎隆之, 森健一郎, 本村亘, 松田泰幸, 黄仁秀, 吉田逸朗, 金然旭, 鈴木定彦, 若宮伸隆

    第48回補体シンポジウム 

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    Event date： 2011.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：名古屋  

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  • An arthropod cuticular chitin-binding protein endows injured sites with transglutaminase-dependent mesh

    Yasuyuki Matsuda, Takumi Koshiba, Tsukasa Osaki, Haruka Suyama, Fumio Arisaka, Yoshihiro Toh, Shun-ichiro Kawabata

    BMB2007 (第30回日本分子生物学会年会・第80回日本生化学会大会) 

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    Event date： 2007.12

    Language：English   Presentation type：Symposium, workshop panel (public)  

    Venue：横浜  

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  • カブトガニ外皮タンパク質（カラキシン）は、トランスグルタミナーゼによって架橋され網目状繊維を形成する

    松田泰幸, 尾崎 司, 小柴琢己, 有坂文雄, 川畑俊一郎

    第7回日本蛋白質科学会年会 

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    Event date： 2007.5

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：仙台  

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  • Characterization of caraxin-1, a horseshoe crab cuticular protein for transglutaminase-dependent protein cross-linking

    Yasuyuki Matsuda, Tsukasa Osaki, Takumi Koshiba, Fumio Arisaka, Shun-ichiro Kawabata

    文部科学省科学研究費 特定領域研究 平成18年度公開シンポジウム 自然免疫による異物認識の分子基盤 

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    Event date： 2006.8

    Language：English   Presentation type：Oral presentation (general)  

    Venue：福岡  

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  • Characterization of a recombinant caraxin-1, a horseshoe crab cuticular protein for transglutaminase-dependent cross-linking

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    Event date： 2005.10

    Language：Japanese   Presentation type：Oral presentation (general)  

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  • Cuticular chitin-binding proteins from horseshoe crab exoskeleton are involved in transglutaminase-dependent cross-linking

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    Event date： 2005.10

    Language：Japanese   Presentation type：Oral presentation (general)  

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  • カブトガニ外骨格キチン結合タンパク質はトランスグルタミナーゼによって架橋される

    飯島学, 松田泰幸, 川畑俊一郎

    第29回蛋白質と酵素の構造と機能に関する九州シンポジウム 

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    Event date： 2005.9

    Language：Japanese   Presentation type：Poster presentation  

    Venue：福岡  

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  • カブトガニ外骨格のトランスグルタミナーゼ基質の構造機能解析

    松田泰幸, 尾崎司, 小柴琢己, 川畑俊一郎

    第29回蛋白質と酵素の構造と機能に関する九州シンポジウム 

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    Event date： 2005.9

    Language：Japanese   Presentation type：Poster presentation  

    Venue：福岡  

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  • Comprehensive sequence analysis of horseshoe crab cuticular proteins and their involvement in transglutaminase-dependent cross-linking

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    Event date： 2005.8

    Presentation type：Oral presentation (general)  

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  • カブトガニ外骨格のトランスグルタミナーゼ基質の構造機能解析

    松田泰幸, 尾崎司, 小柴琢己, 川畑俊一郎

    第5回日本蛋白質科学会年会 

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    Event date： 2005.6 - 2005.7

    Language：Japanese   Presentation type：Poster presentation  

    Venue：福岡  

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  • Characterization of a transglutaminase substrate identified from cuticular chitin-binding proteins in horseshoe crabs

    Yasuyuki Matsuda, Tsukasa Osaki, Shun-ichiro Kawabata

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    Event date： 2004.10

    Language：Japanese   Presentation type：Oral presentation (general)  

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  • Characterization of a transglutaminase substrate identified from cuticular chitin-binding proteins in horseshoe crabs

    Yasuyuki Matsuda, Tsukasa Osaki, Shun-ichiro Kawabata

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    Event date： 2004.9

    Language：English   Presentation type：Oral presentation (general)  

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  • カブトガニ血球トランスグルタミナーゼの血リンパ凝固および自然免疫における役割

    尾崎司, 松田泰幸, 橋本倫徳, 飯島学, 川畑俊一郎

    第76回日本生化学会大会 

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    Event date： 2003.10

    Presentation type：Oral presentation (general)  

    Venue：横浜  

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  • インテグリン活性化におけるintegrin-linked kinaseの役割

    本田繁則, 池島裕子, 松田泰幸, 田所誠司, 冨山佳昭, 宮田敏行

    第72回日本血液学会学術集会  2010.9 

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    Presentation type：Poster presentation  

    Venue：横浜  

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  • Role of ILK-PINCH-parvin complex in supporting functional expression of integrin International conference

    XXIII Congress of The International Society on Thrombosis and Haemostasis  2011.7 

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  • An RNAi screening to identify the molecules involved in integrin αIIbβ3 activation International conference

    XXIII Congress of The International Society on Thrombosis and Haemostasis  2011.7 

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  • カブトガニ外皮タンパク質カラキシンは、創傷部位においてトランスグルタミナーゼによって架橋され、網目状繊維を形成する

    松田泰幸, 小柴琢己, 尾崎司, 陶山晴香, 有坂文雄, 藤義博, 川畑俊一郎

    日本比較免疫学会第19回学術集会  2007.8 

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    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：浜松  

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  • An arthropod cuticular chitin-binding protein endows injured sites with transglutaminase-dependent mesh

    Yasuyuki Matsuda, Takumi Koshiba, Tsukasa Osaki, Haruka Suyama, Fumio Arisaka, Yoshihiro Toh, Shun-ichiro Kawabata

    第2回 トランスグルタミナーゼ研究会・ポリアミン学会 合同学術集会  2007.12 

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    Language：Japanese   Presentation type：Poster presentation  

    Venue：東京  

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  • コレクチンCL-L1の組織局在と分子構造に関する解析

    松田泰幸, ロイ・ニタイ, 森健一郎, 黄仁秀, 大谷克城, 若宮伸隆

    第86回日本生化学会大会  2013.9 

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    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：横浜  

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  • In vitro and in vivo roles in Collectin Kidney 1 (CL-K1) with innate immunity against Streptcoccus pneumoniae

    Insu Hwang, Kenichiro Mori, Katsuki Ohtani, Yasuyuki Matsuda, Nitai Roy, YounUck Kim, Nobutaka Wakamiya

    26th International Complement Workshop  2016.9 

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  • 膜型コレクチンCL-P1は、CRPを介して補体経路を活性化する

    ロイ・ニタイ, 大谷克城, 松田泰幸, 森健一郎, 黄仁秀, 井上徳光, 若宮伸隆

    第89回日本生化学会大会  2016.9 

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    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：仙台  

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  • 新規コレクチンCL-K1は、マウスにおける肺炎球菌感染に対して防御的に働く

    黄仁秀, 森健一郎, 大谷克城, 松田泰幸, ロイ・ニタイ, 若宮伸隆

    第89回日本生化学会大会  2016.9 

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    Venue：仙台  

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  • Structural characterization of novel collectins, CL-L1, CL-K1, and CL-LK in blood International conference

    Yasuyuki Matsuda, Katsuki Ohtani, Nitai Roy, Insu Hwang, Kenichiro Mori, Nobutaka Wakamiya

    26th International Complement Workshop  2016.9 

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  • Collectin CL-P1 is involved in C-reactive protein-mediated complement activation International conference

    Nitai Roy, Katsuki Ohtani, Yasuyuki Matsuda, Kenichiro Mori, Insu Hwang, Yasuhiko Suzuki, Norimitsu Inoue, Nobutaka Wakamiya

    26th International Complement Workshop  2016.9 

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  • スカベンジャー受容体CL-P1は、Pentraxinを介して補体系を活性化する

    ロイ・ニタイ, 大谷 克城, 日高 義彦, 天野 芳郎, 松田 泰幸, 森 健一郎, 黄 仁秀, 井上 徳光, 若宮 伸隆

    第54回日本補体学会学術集会  2017.9 

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    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：福島  

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  • コレクチンCL-LKはDNAに結合して補体系を活性化する

    松田泰幸, 大谷克城, ロイ・ニタイ, 森健一郎, 黄仁秀, 若宮伸隆

    2017年度生命科学系学会合同年次大会 (第40回日本分子生物学会年会、第90回日本生化学会大会)  2017.12 

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    Language：Japanese   Presentation type：Poster presentation  

    Venue：神戸  

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  • コレクチンCL-K1の生化学的解析

    大谷克城, 森健一郎, 黄仁秀, 吉崎隆之, 松田泰幸, ロイ・ニタイ, 若宮伸隆

    第33回日本糖質学会年会  2014.8 

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    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：名古屋  

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  • コレクチンCL-K1の生体防御機能に関する検討

    黄仁秀, 森健一郎, 松田泰幸, ロイ・ニタイ, 大谷克城, 若宮伸隆

    第51回補体シンポジウム  2014.8 

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    Venue：神戸  

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  • コレクチンCL-K1の凝固系への関与について

    大谷克城, Takahashi Kazue, 早川峰司, 森健一郎, 黄仁秀, 吉崎隆之, 松田泰幸, ロイ・ニタイ, 丸藤哲, 若宮伸隆

    第87回日本生化学会大会  2014.10 

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    Language：Japanese   Presentation type：Poster presentation  

    Venue：京都  

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  • 新規コレクチンCL-K1と相互作用する血漿由来タンパク質の同定

    松田泰幸, 大谷克城, 森健一郎, ロイ・ニタイ, 黄仁秀, 若宮伸隆

    第34回日本糖質学会年会  2015.7 

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    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：東京  

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  • 日本人に高頻度に見られるプラスミノーゲン栃木変異をもつ遺伝子改変マウスの血栓傾向の解析

    田嶌優子, 坂野史明, 喜多俊行, 松田泰幸, 柳本広二, 宮田敏行

    第19回日本病態プロテアーゼ学会学術集会  2014.8 

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    Venue：大阪  

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  • コレクチンCL-P1は、急性期タンパクCRPを介して補体経路を活性化する

    大谷克城, ロイ・ニタイ, 松田泰幸, 森健一郎, 黄仁秀, 井上徳光, 若宮伸隆

    第35回日本糖質学会年会  2016.9 

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    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：高知  

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  • 新規コレクチン CL-K1 の糖鎖認識と生物学的活性についての解析

    大谷克城, Umakhanth Venkatraman Girija, 森健一郎, 吉崎隆之, 松田泰幸, 黄仁秀, Nitai Roy, Russell Wallis, 若宮伸隆

    第34回日本糖質学会年会  2015.7 

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    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：東京  

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  • CL-K1 は、肺炎球菌感染に対し、補体レクチン経路を介して生体防御に機能する

    黄仁秀, 森健一郎, 松田泰幸, ロイ・ニタイ, 大谷克城, 若宮伸隆

    第34回日本糖質学会年会  2015.8 

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    Language：Japanese   Presentation type：Poster presentation  

    Venue：東京  

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  • スカベンジャー受容体CL-P1は、CRPを介して古典的経路を活性化する

    ロイ・ニタイ, 大谷克城, 松田泰幸, 森健一郎, 黄仁秀, 若宮伸隆

    第52回日本補体学会学術集会  2015.8 

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    Presentation type：Oral presentation (general)  

    Venue：名古屋  

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  • コレクチンCL-K1の糖鎖認識と3MC症候群における変異の分子機構への影響

    大谷克城, Umakhanth Venkatraman Girija, 森健一郎, 吉崎隆之, 松田泰幸, 黄仁秀, ロイ・ニタイ, Russell Wallis, 若宮伸隆

    BMB2015 (第38回日本分子生物学会年会・第88回日本生化学会大会)  2015.12 

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    Presentation type：Poster presentation  

    Venue：神戸  

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  • コレクチンCL-K1の組織における発現検討

    大谷克城, 本村亘, 吉崎孝之, 森健一郎, 松田泰幸, 黄仁秀, ロイ・ニタイ, 吉田逸朗, 鈴木定彦, 若宮伸隆

    第49回補体シンポジウム  2012.8 

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    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：大阪  

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  • コレクチンCL-K1のマウスおよびヒト組織における発現検討

    大谷克城, 本村亘, 吉崎隆之, 森健一郎, 松田泰幸, 黄仁秀, ロイ・ニタイ, 吉田逸朗, 鈴木定彦, 若宮伸隆

    第31回日本糖質学会  2012.9 

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    Language：Japanese   Presentation type：Poster presentation  

    Venue：鹿児島  

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  • マウスプラスミノーゲン栃木変異は血漿プラスミン活性を低下させるが血栓塞栓症の原因にはならない

    田嶌優子, 坂野史明, 喜多俊行, 松田泰幸, 柳本広二, 宮田敏行

    第86回日本生化学会大会  2013.9 

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    Presentation type：Poster presentation  

    Venue：横浜  

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  • コレクチンCL-K1の生体防御機能に関する検討

    黄仁秀, 森健一郎, 松田泰幸, ロイ・ニタイ, 大谷克城, 若宮伸隆

    第79回日本インターフェロン・サイトカイン学会学術集会  2014.6 

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    Language：Japanese   Presentation type：Poster presentation  

    Venue：札幌  

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  • コレクチンCL-L1の組織局在と分子構造に関する解析

    松田泰幸, ロイ・ニタイ, 森健一郎, 黄仁秀, 大谷克城, 若宮伸隆

    第50回補体シンポジウム  2013.7 

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    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：旭川  

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  • コレクチンCL-L1の組織局在と分子構造に関する解析

    松田泰幸, ロイ・ニタイ, 森健一郎, 黄仁秀, 大谷克城, 若宮伸隆

    第32回日本糖質学会年会  2013.8 

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    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：大阪  

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Awards

  • JSTH Asian-Pacific Scholarship

    2011.7   International Society on Thrombosis and Haemostasis  

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  • 古田奨励賞

    2007.8   日本比較免疫学会  

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Research Projects

  • コレクチン複合体CL-LKが3MC症候群の病態に与える影響とその分子基盤の解明

    Grant number：18K06947  2018.4 - 2022.3

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    松田 泰幸

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    Grant amount：\4,550,000 （ Direct Cost: \3,500,000 、 Indirect Cost：\1,050,000 ）

    CL-K1は、カルシウム要求性のレクチンであり、これまで自然免疫に関与することが報告されてきたが、ヒトの形態形成に異常をきたす遺伝病（3MC症候群）の患者からコレクチンCL-K1の遺伝的変異が報告されたことにより、CL-K1が自然免疫のみならず、個体発生や成長発育に関わる可能性が示唆されている。また、CL-K1が別のコレクチンCL-L1とヘテロ複合体を形成していることを明らかにしたが、詳細な分子機構は未だ不明である。本研究では、CL-K1およびCL-L1の新規機能を明らかにすることで、3MC症候群の発症原因や発症機序を明らかにするとともに、本疾患の治療法開発に向けた知見の集積を目指す。
    令和元年度は、前年度に作製したCL-L1およびCL-K1発現コンストラクトから組換えバキュロウイルスを得た。このバキュロウイルスを昆虫細胞（Sf9細胞）に感染させタンパク質発現を行った。ウェスタンブロットを用いて、感染後Sf9細胞培養上清のCL-L1およびCL-K1の検出を試みたところ、どちらも培養上清中に発現していることが確認できた。この培養上清から、CL-L1、CL-K1に付加されているタグを利用して、タンパク質の精製を行ったところ、ウェスタンブロットで溶出画分からCL-K1およびCL-L1を検出することができたが、CBB染色でバンドを確認できる程の収量ではなかった。次に、CL-L1とCL-K1の２つを１つの感染細胞内で発現できる組換えバキュロウイルスを作製し、同様にウェスタンブロットで発現を確認したところ、CL-L1、CL-K1ともに感染後のSf9細胞培養上清から検出することができた。しかし、CL-L1あるいはCL-K1を単独で発現させた培養上清に比べて、ウェスタンブロットによるCL-L1、CL-K1検出シグナルがかなり弱く、共発現時の発現量が単独発現に比べて少ないと考えられた。

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  • The development of complement analysis system for complement diseases

    Grant number：17H04108  2017.4 - 2020.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)  Grant-in-Aid for Scientific Research (B)

    wakamiya nobutaka

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    Grant amount：\17,810,000 （ Direct Cost: \13,700,000 、 Indirect Cost：\4,110,000 ）

    In late years、the participation of the complement activation is doubted for an intractable disease. However, the details are unidentified now because the appropriate analysis of the complement factor relating the disease condition of a patient to complement activation and the system do not exist. We will build the purpose of this study with development of the new complement activation system of measurement, and re-builds up the pro-standard analysis complement activation resolvent system of measurement and is to elucidate the complement activation condition of a patient mechanism of the complement-related disease. As result, we established complement factor assay system for ten items that could measure C3, C4, CH50, Ba, sC5b9, C5a, CFH, CFI, C1-INH activity, CFH-IgG and devised the standard value of these ten items and announced it with an official journal of a complement scientific society "Hotai" in December, 2019.

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  • 新規コレクチンCL-K1の精製法の確立およびCL-K1相互作用分子の探索

    2016.6 - 2017.9

    松田泰幸

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\500,000

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  • Study on the involvement of collectin CL-K1 in the pathogenesis of 3MC syndrome and elucidation of its molecular mechanism

    Grant number：16K19045  2016.4 - 2019.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)  Grant-in-Aid for Young Scientists (B)

    Matsuda Yasuyuki

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    Grant amount：\3,900,000 （ Direct Cost: \3,000,000 、 Indirect Cost：\900,000 ）

    The association between the gene defect of collectin CL-K1 and the pathology of 3MC syndrome has been found, suggesting that CL-K1 may be involved in growth and development. The purpose of this study is to elucidate the pathogenesis of 3MC syndrome in order to explore the possibility of establishing a medical treatment for it. I found that CL-K1 interacts with collectin CL-L1, suggesting that CL-L1 may also be related to the pathogenesis of 3MC syndrome.

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  • コレクチンCL-K1の相互作用分子の探索と機能の解明

    2015.10 - 2016.9

    松田泰幸

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\750,000

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  • The role of CL-K1 in DIC patients

    Grant number：26293124  2014.4 - 2018.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)  Grant-in-Aid for Scientific Research (B)

    WAKAMIYA NOBUTAKA

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    Grant amount：\16,510,000 （ Direct Cost: \12,700,000 、 Indirect Cost：\3,810,000 ）

    In collectin CL-K1 which Wakamiya discovered, it is supposed as well as conventional collectin that I have a natural immunity function. I performed DIC patient registration and performed sample collection of blood. I measured the inspection item of the DIC mainly on solidification fibrinolysis system. On the other hand, about collectin, I narrowed it down to two of CL-K1 and MBL. In the previous study, CL-K1 took the value that related to in progress of the DIC. However, in the measurement of this Japanese, the meaningful difference was not seen in presence of the DIC.

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  • コレクチンCL-L1の分子構造と組織局在に関する解析

    2013.10 - 2014.9

    松田泰幸

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\500,000

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  • Basic study of evaluation system in vascular diseases

    Grant number：22390113  2010 - 2012

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)  Grant-in-Aid for Scientific Research (B)

    WAKAMIYA Nobutaka, OHTANI Katsuki, SUZUKI Ysuhiko, YOSHIDA Itsuro, MORI Kenichiro, MATSUSHITA Misao, MATSUDA Yasuyuki

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    Grant amount：\17,550,000 （ Direct Cost: \13,500,000 、 Indirect Cost：\4,050,000 ）

    The basic study of CL-P1 and CL-K1 has been performed by using recombinant collectins and gene-modified mice. Both established recombinant collectins could produce their antibodies, which were used for the development of ELISA system and evaluation of tissue expressions in those mice and human. The knock-out mice with CL-P1 and CL-K1 have been established. CL-K1 KO mice were analyzed using above antibodies. The prototype ELISA system for the evaluation of its blood concentration was established. The CL-P1 KO and TG mice have been established and their complementation experiments have been performed.

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  • 血小板凝集の機能調節に関わる分子のクローニングとその機能解析

    Grant number：09J08544  2009 - 2011

    日本学術振興会  科学研究費助成事業 特別研究員奨励費  特別研究員奨励費

    松田 泰幸

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    Grant amount：\2,800,000 （ Direct Cost: \2,800,000 ）

    血小板凝集は止血機能を果たしており、生命維持において重要であるが、過剰な凝集は病的な血栓を形成して様々な循環器疾患(脳梗塞、心筋梗塞など)を引き起こす原因にもなる。血小板凝集にはインテグリンα_<IIb>β_3の活性化が関与しているため、本研究ではヒトの活性型インテグリンを発現させたCHO細胞を用いてインテグリンα_<IIb>β_3の活性化メカニズムに関わる新規シグナル分子の探索及び機能解析をおこなった。
    2年目である今年度は、PAC-1結合能が低下した変異CHO細胞株にcDNAライブラリを導入し、インテグリンα_<IIb>β_3の活性化に関わる分子のクローニングを試みた。インテグリンの活性化の指標には、ヒトの活性型インテグリンα_<IIb>β_3を認識するPAC-1抗体を用いた。cDNAライブラリを導入後、PAC-1結合能が回復した細胞をCell Sorterを用いて回収し、細胞から導入されたcDNAを回収することで、インテグリンα_<IIb>β_3の活性化に関わるcDNAの特定を試みた。しかし、今回単離した2種類の変異CHO細胞株では、回収したcDNAを変異CHO細胞に再導入してもPAC-1結合能の回復がみられず、インテグリンα_<IIb>β_3の活性化に関わる分子の特定はできなかった。また、今年度はsiRNAライブラリを用いてインテグリンα_<IIb>β_3の活性化に関わる新規分子の同定を試みた。マウスあるいはラットに対するsiRNAライブラリ計590個のsiRNAをそれぞれCHO細胞株に導入してスクリーニングをおこない、PAC-1結合能を70%以下に抑制するsiRNAを54個得ることに成功した。この結果はインテグリンα_<IIb>β_3の活性化メカニズムに関わる新規シグナル分子の存在を示唆するものである。チャイニーズハムスターに対するsiRNAの設計を行い、さらなる検討を行う必要性がある。

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Teaching Experience

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Social Activities

  • わくわくサイエンス in サイパル

    Role(s)： Planner,　Organizing member

    2020.2

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    Type：Other

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  • HOKKAIDOサイエンスセミナー for Students Ⅳ「医学研究アラカルト」

    Role(s)： Lecturer

    2019.11

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    Type：Seminar, workshop

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