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Affiliation |
Faculty of Medicine School of Medicine Department of Medical Sciences, Vascular and cellular dynamics |
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Professor |
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Laboratory Address |
5200 Kihara, Kiyotake-cho, Miyazaki-city, Miyazaki 889-1692 |
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Laboratory Phone number |
+81-985-85-0985 |
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Contact information |
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Homepage |
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External Link |
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Related SDGs |
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NISHIYAMA Koichi
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Research Interests 【 display / non-display 】
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Live imaging
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Angiogenesis
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vascular basement membrane
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微小血管ネットワーク
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Vascular endothelial cell
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Blood flow
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Mathematical model
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Quantitative analysis
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Mechanical stimuli
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pericyte
Research Areas 【 display / non-display 】
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Life Science / Biophysics
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Life Science / Biomedical engineering
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Life Science / Cell biology
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Life Science / Molecular biology
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Life Science / Cardiology
Education 【 display / non-display 】
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Kumamoto University Faculty of Medicine
- 1992.4
Campus Career 【 display / non-display 】
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University of Miyazaki Faculty of Medicine School of Medicine Department of Medical Sciences, Vascular and cellular dynamics Professor
2021.06 - Now
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University of Miyazaki Faculty of Medicine School of Medicine Function control study course tumor biochemistry field Professor
2021.04 - 2021.05
External Career 【 display / non-display 】
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Kumamoto University Lecturer
2014.4 - 2016.3
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Kumamoto University International Research Center for Medical Sciences Chief Researcher
2014 - 2021.3
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The University of Tokyo Graduate School of Medicine Assistant Professor
2006.4 - 2014.3
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The University of Tokyo Graduate School of Medicine Researcher
2005.4 - 2006.3
Professional Memberships 【 display / non-display 】
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日本発生生物学会
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日本血管生物医学会
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日本癌学会
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日本生化学会
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日本生体医工学会
Papers 【 display / non-display 】
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Mechanical loading of intraluminal pressure mediates wound angiogenesis by regulating the TOCA family of F-BAR proteins. Reviewed International coauthorship International journal
Shinya Yuge, Koichi Nishiyama, Yuichiro Arima, Yasuyuki Hanada, Eri Oguri-Nakamura, Sanshiro Hanada, Tomohiro Ishii, Yuki Wakayama, Urara Hasegawa, Kazuya Tsujita, Ryuji Yokokawa, Takashi Miura, Toshiki Itoh, Kenichi Tsujita, Naoki Mochizuki, Shigetomo Fukuhara
Nature communications 13 ( 1 ) 2594 - 2594 2022.12
Authorship：Lead author, Corresponding author Language：English Publishing type：Research paper (scientific journal)
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Biomechanical control of vascular morphogenesis by the surrounding stiffness Reviewed
花田 保之, 小河 穂波, 西山 功一
Nature Communications 16 6788 2025.7
Language：English Publishing type：Research paper (scientific journal) Publisher：Springer Nature
Sprouting angiogenesis is a form of morphogenesis which expands vascular networks from preexisting networks. However, the precise mechanism governing efficient branch elongation driven by directional movement of endothelial cells (ECs), while the lumen develops under the influence of blood inflow, remains unknown. Herein, we show perivascular stiffening to be a major factor that integrates branch elongation and lumen development. The lumen expansion seen during lumen development inhibits directional EC movement driving branch elongation. This process is counter-regulated by the presence of pericytes, which induces perivascular stiffening by promoting the deposition of EC-derived collagen-IV (Col-IV) on the vascular basement membrane (VBM), thereby preventing excessive lumen expansion. Furthermore, inhibition of forward directional movement of the tip EC during lumen development is associated with decreased localization of the F-BAR proteins and Arp2/3 complexes at the leading front. Our results demonstrate how ECs elongate branches, while the lumen develops, by properly building the surrounding physical environment in coordination with pericytes during angiogenesis.
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Biomechanical control of vascular morphogenesis by the surrounding stiffness. Reviewed International journal
Yasuyuki Hanada, Semanti Halder, Yuichiro Arima, Misato Haruta, Honami Ogoh, Shuntaro Ogura, Yukihiko Shiraki, Sota Nakano, Yuka Ozeki, Shigetomo Fukuhara, Akiyoshi Uemura, Toyoaki Murohara, Koichi Nishiyama
Nature communications 16 ( 1 ) 6788 - 6788 2025.7
Authorship：Corresponding author Language：English Publishing type：Research paper (scientific journal)
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第1土曜特集 "かたちづくり" を制御する分子メカニズム 形態形成と多細胞動態 血管新生における血流による物理的力の役割 Invited
花田 保之, 西山 功一
医学のあゆみ 290 ( 1 ) 42 - 46 2024.7
Language：Japanese Publishing type：Part of collection (book) Publisher：医歯薬出版
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第5土曜特集 血管･リンパ管研究の最前線と治療への展開 血管研究のフロンティア 再構成解析系を駆使した血流による血管新生の生体力学機序の解明 Invited
西山 功一
医学のあゆみ 289 ( 13 ) 1093 - 1098 2024.6
Authorship：Lead author, Corresponding author Language：Japanese Publishing type：Part of collection (book) Publisher：医歯薬出版
MISC 【 display / non-display 】
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血流に起因する内腔圧による創傷治癒過程の血管新生の新たな制御機構
福原茂朋, 弓削進弥, 西山功一, 有馬勇一郎, 花田保之, 花田三四郎, 石井智裕, 若山勇紀, 辻田和也, 横川隆司, 三浦岳, 望月直樹
日本生化学会大会(Web) 93rd 2020
Authorship：Lead author Language：Japanese Publishing type：Rapid communication, short report, research note, etc. (scientific journal)
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花田 保之, 西山 功一
医学のあゆみ 290 ( 1 ) 42 - 46 2024.7
Language：Japanese Publishing type：Article, review, commentary, editorial, etc. (scientific journal) Publisher：東京 : 医歯薬出版
Other Link： https://ndlsearch.ndl.go.jp/books/R000000004-I033576985
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創傷治癒過程の血管新生における内腔圧の新たな役割の解明 Invited
福原茂朋, 弓削進弥, 有馬勇一郎, 花田保之, 花田三四郎, 石井智裕, 若山勇紀, 横川隆司, 三浦岳, 望月直樹, 西山功一
脈管学(Web) 60 ( supplement ) 2020
Language：Japanese Publishing type：Research paper, summary (national, other academic conference)
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内腔圧の機械的刺激により制御される創傷治癒での血管新生
弓削進弥, 西山功一, 有馬勇一郎, 花田保之, 花田三四郎, 石井智裕, 若山勇紀, 辻田和也, 横川隆司, 三浦岳, 望月直樹, 福原茂朋
日本生化学会大会(Web) 93rd 2020
Language：Japanese Publishing type：Rapid communication, short report, research note, etc. (scientific journal)
Grant-in-Aid for Scientific Research 【 display / non-display 】
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Elucidation of the biomechanical control mechanism of angiogenesis through integration of blood flow action by pericytes
Grant number：24K03267 2024.04 - 2027.03
Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)
Authorship：Principal investigator
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Development of an in vitro reconstitution method for reproducing human kidney glomerular structure and function by vascularization and perfusion of organoid
Grant number：24K22384 2024.04 - 2027.03
Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Research (Exploratory)
Authorship：Principal investigator
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Angiogenic machinery via concerted biomechanical control by blood flow pericyte
Grant number：19H04446 2021.04 - 2024.03
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)
Nishiyama Koichi
Authorship：Principal investigator
Once blood vessel is damaged, it is repaired by angiogenesis. In this study, we recovered that angiogenesis is suppressed by intravascular pressure caused by blood flow. In addition, we uncovered the molecular mechanism of how vascular endothelial cells composing angiogenic sprouts sense vascular wall tension generated by intravascular pressure load to suppress angiogenesis. We further uncovered that perivascular pericytes adjust vascular dilation-caused suppression of angiogenesis and angiogenesis is controlled coordinately by blood flow and pericytes.
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Reproduction of kidney glomerulus structure and function using human iPS cells-derived organoid and vascular chip
Grant number：21K19487 2021.04 - 2023.03
Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Research (Exploratory) Grant-in-Aid for Challenging Research (Exploratory)
Authorship：Principal investigator
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Cellular and molecular mechanisms underlying inflammation and fibrosis in pericyte-deficient retinai
Grant number：19H03437 2019.04 - 2022.03
Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)
Uemura Akiyoshi
Authorship：Coinvestigator(s)
By intraperitoneally injecting an anti-PDGFRβ monoclonal antibody (clone APB5) to neonatal mice, we previously established a pericyte-deficient retinopathy model, which reproduced retinal vascular disorders characteristic to diabetic retinopathy. In the present study, we elucidated that mononuclear phagocytes infiltrating around the pericyte-free retinal vessels were derived from both activated microglia and monocyte-derived macrophages. After the onset of retinal detachment caused by the hyperpermeability of the pericyte-free retinal vessels, activated microglia accumulated in the subretinal spaces and induced fibrosis. In these fibrotic tissues, myofibroblasts were derived both pericytes and retinal pigment epithelium cells.
Available Technology 【 display / non-display 】
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血管新生のしくみの解明と医療応用
物流ネットワークとしての血管形成とその破綻による病気の理解と制御
血流がある生命現象の試験管内モデルの開発と医学・薬学への応用Home Page： 医学部機能制御学講座血管動態制御学分野
Related fields where technical consultation is available：1．血管新生の解析全般 2．タイムラプスイメージングによる分子・細胞動態の定量的解析 3．ホールマウント免疫染色と画像解析、定量化 4．血管チップを使ったオルガノイド、組織の培養 5．血管チップを使った力学刺激の評価、医療応用
Message：医学・生物学にとらわれない視点で、多くの共同研究者とともに学際的な研究を推進しています。興味を持たれた方はお気軽にお声掛けください。