論文

査読有り
1999年4月

Signaling transduction pathway of angiotensin II in human mesangial cells: Mediation of focal adhesion and GTPase activating proteins

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
  • Y Shikata
  • ,
  • K Shikata
  • ,
  • M Masuda
  • ,
  • H Sugimoto
  • ,
  • J Wada
  • ,
  • H Makino

257
1
開始ページ
234
終了ページ
238
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1006/bbrc.1999.0441
出版者・発行元
ACADEMIC PRESS INC ELSEVIER SCIENCE

Human mesangial cells (HMCs) respond to angiotensin II stimulation, which modulates their physiological activities, i.e., contraction and proliferation. It has been revealed that focal adhesion kinase (FAK) and paxillin participate in the angiotensin Ii-mediated signaling and cytoskeletal rearrangements at focal adhesion. We investigated the influences of cell adhesion upon angiotensin LI effects in HMCs. In adherent cells, both FAR and paxillin were tyrosine phosphorylated by angiotensin II, while the cell detachment completely inhibited the tyrosine phosphorylation of paxillin. Activation of p44/42 mitogen-activated protein (MAP) kinase by angiotensin II was accentuated in suspended cells. Moreover, p190, a member of Rho GTPase activating protein (GAP), and RasGAP were coprecipitated with paxillin in adherent cells and angiotensin II stimulation reduced the formation of paxillin-p190 and paxillin-RasGAP complexes. These results suggest that the formation of focal adhesion complexes accelerated by accumulation of mesangial matrices may inhibit the proliferation of HMCs by modulating MAP kinase activity and be related to mesangial cell depletion. (C) 1999 Academic Press.

リンク情報
DOI
https://doi.org/10.1006/bbrc.1999.0441
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000079615100040&DestApp=WOS_CPL
URL
http://orcid.org/0000-0003-1468-5170
ID情報
  • DOI : 10.1006/bbrc.1999.0441
  • ISSN : 0006-291X
  • ORCIDのPut Code : 17913159
  • Web of Science ID : WOS:000079615100040

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