NISHIYAMA Koichi

写真a

Affiliation

Faculty of Medicine School of Medicine Department of Medical Sciences, Vascular and cellular dynamics

Title

Professor

Laboratory Address

5200 Kihara, Kiyotake-cho, Miyazaki-city, Miyazaki 889-1692

Laboratory Phone number

+81-985-85-0985

Contact information

Contact information

Homepage

https://kumamoto-ircms-nishiyama.jp/en/

External Link

Degree 【 display / non-display

  • MD, PhD ( 2006.2   Kumamoto University )

Research Interests 【 display / non-display

  • vascular basement membrane

  • 微小血管ネットワーク

  • Angiogenesis

  • Vascular endothelial cell

  • Blood flow

  • Mathematical model

  • Quantitative analysis

  • Mechanical stimuli

  • Live imaging

  • pericyte

Research Areas 【 display / non-display

  • Life Science / Biomedical engineering

  • Life Science / Cell biology

  • Life Science / Molecular biology

  • Life Science / Pathological biochemistry

  • Life Science / Biophysics

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Education 【 display / non-display

  • Kumamoto University   Faculty of Medicine

    - 1992.4

Campus Career 【 display / non-display

  • University of Miyazaki   Faculty of Medicine   School of Medicine   Department of Medical Sciences, Vascular and cellular dynamics   Professor

    2021.06 - Now

  • 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

  • Kumamoto University   Lecturer

    2014.4 - 2016.3

  • Kumamoto University   International Research Center for Medical Sciences   Chief Researcher

    2014 - 2021.3

  • The University of Tokyo   Graduate School of Medicine   Assistant Professor

    2006.4 - 2014.3

  • The University of Tokyo   Graduate School of Medicine   Researcher

    2005.4 - 2006.3

Professional Memberships 【 display / non-display

  • 日本発生生物学会

  • 日本血管生物医学会

  • 日本癌学会

  • 日本生化学会

  • 日本生体医工学会

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Papers 【 display / non-display

  • NFAT indicates nucleocytoplasmic damped oscillation via its feedback modulator Reviewed

    Masashi Muramatsu, Takeshi Ito, Hokuto Shimoji, Miko Komiya, Yuri Miyamura, Koichi Nishiyama, Takashi Suzuki, Takashi Minami

    Biochemical and Biophysical Research Communications   571   201 - 209   2021.9

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

    DOI: 10.1016/j.bbrc.2021.07.072

    PubMed

  • Dysregulation of Amphiregulin stimulates the pathogenesis of cystic lymphangioma Reviewed International coauthorship

    Yoshida N., Yamamoto S., Hamashima T., Okuno N., Okita N., Horikawa S., Hayashi M., Dang T.C., Nguyen Q.L., Nishiyama K., Makinod T., Ishii Y., Tomihara K., Shimizu T., Shibuya M., Noguchi M., Sasahara M.

    Proceedings of the National Academy of Sciences of the United States of America   118 ( 19 )   2021.5

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Proceedings of the National Academy of Sciences of the United States of America  

    Along with blood vessels, lymphatic vessels play an important role in the circulation of body fluid and recruitment of immune cells. Postnatal lymphangiogenesis commonly occurs from preexisting lymphatic vessels by sprouting, which is induced by lymphangiogenic factors such as vascular endothelial growth factor C (VEGF-C). However, the key signals and cell types that stimulate pathological lymphangiogenesis, such as human cystic lymphangioma, are less well known. Here, we found that mouse dermal fibroblasts that infiltrate to sponges subcutaneously implanted express VEGF-D and sushi, Von Willebrand factor type A, EGF, and pentraxin domain containing 1 (SVEP1) in response to PDGFRβ signal. In vitro, Pdgfrb knockout (β-KO) fibroblasts had reduced expression of VEGF-D and SVEP1 and overproduced Amphiregulin. Dysregulation of these three factors was involved in the cyst-like and uneven distribution of lymphatic vessels observed in the β-KO mice. Similarly, in human cystic lymphangioma, which is one of the intractable diseases and mostly occurs in childhood, fibroblasts surrounding cystic lymphatics highly expressed Amphiregulin. Moreover, fibroblastderived Amphiregulin could induce the expression of Amphiregulin in lymphatic endothelial cells. The dual source of Amphiregulin activated EGFR expressed on the lymphatic endothelial cells. This exacerbation cascade induced proliferation of lymphatic endothelial cells to form cystic lymphangioma. Ultimately, excessive Amphiregulin produced by fibroblasts surrounding lymphatics and by lymphatic endothelial cells per se results in pathogenesis of cystic lymphangioma and will be a fascinating therapeutic target of cystic lymphangioma.

    DOI: 10.1073/pnas.2019580118

    Scopus

    PubMed

  • Murine neonatal ketogenesis preserves mitochondrial energetics by preventing protein hyperacetylation Reviewed

    Yuichiro Arima, Yoshiko Nakagawa, Toru Takeo, Toshifumi Ishida, Toshihiro Yamada, Shinjiro Hino, Mitsuyoshi Nakao, Sanshiro Hanada, Terumasa Umemoto, Toshio Suda, Tetsushi Sakuma, Takashi Yamamoto, Takehisa Watanabe, Katsuya Nagaoka, Yasuhito Tanaka, Yumiko K. Kawamura, Kazuo Tonami, Hiroki Kurihara, Yoshifumi Sato, Kazuya Yamagata, Taishi Nakamura, Satoshi Araki, Eiichiro Yamamoto, Yasuhiro Izumiya, Kenji Sakamoto, Koichi Kaikita, Kenichi Matsushita, Koichi Nishiyama, Naomi Nakagata, Kenichi Tsujita

    Nature Metabolism   3 ( 2 )   196 - 210   2021.2

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    DOI: 10.1038/s42255-021-00342-6

    Scopus

    PubMed

    Other Link: http://www.nature.com/articles/s42255-021-00342-6

  • A new perfusion culture method with a self-organized capillary network Reviewed

    Kei Sugihara, Yoshimi Yamaguchi, Shiori Usui, Yuji Nashimoto, Sanshiro Hanada, Etsuko Kiyokawa, Akiyoshi Uemura, Ryuji Yokokawa, Koichi Nishiyama, Takashi Miura

    PLOS ONE   15 ( 10 October )   e0240552 - e0240552   2020.10

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Public Library of Science (PLoS)  

    DOI: 10.1371/journal.pone.0240552

    Scopus

    PubMed

  • RhoJ integrates attractive and repulsive cues in directional migration of endothelial cells Reviewed

    Yoko Fukushima, Koichi Nishiyama, Hiroshi Kataoka, Marcus Fruttiger, Shigetomo Fukuhara, Kohji Nishida, Naoki Mochizuki, Hiroki Kurihara, Shin‐Ichi Nishikawa, Akiyoshi Uemura

    The EMBO Journal   39 ( 12 )   e102930   2020.6

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

    DOI: 10.15252/embj.2019102930

    Scopus

    PubMed

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MISC 【 display / non-display

  • 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

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    Language:Japanese   Publishing type:Rapid communication, short report, research note, etc. (scientific journal)  

    J-GLOBAL

  • 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

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    Language:Japanese   Publishing type:Rapid communication, short report, research note, etc. (scientific journal)  

    J-GLOBAL

Grant-in-Aid for Scientific Research 【 display / non-display

  • 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)

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    Authorship:Principal investigator 

  • 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)

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    Authorship:Principal investigator 

  • ペリサイト消失網膜における炎症と線維化の細胞・分子機構の解明

    Grant number:19H03437  2019.04 - 2022.03

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

    植村 明嘉, 西山 功一

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    Authorship:Coinvestigator(s) 

    抗PDGFRβ抗体を腹腔内に単回投与して、ペリサイトを消失させた新生仔マウス網膜では、①内皮細胞の炎症反応、②内在性ミクログリアの活性化と骨髄由来マクロファージの浸潤、③血管透過性の亢進、④網膜剥離の発症、⑤活性化型ミクログリアの網膜下への移動、⑥急性炎症から慢性炎症への移行、⑦網膜下の線維化が、順に進行する。こうした過程で、抗CSF1R抗体を投与してミクログリアを消失させると、線維化が抑制されることから、網膜下に移行した活性化型ミクログリアが線維化を誘導することが明らかとなった。さらに単細胞RNAseq解析により、線維化誘導ミクログリアがM2極性化していることが明らかとなった。

Available Technology 【 display / non-display