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
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- 巻
- 257
- 号
- 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
- ID情報
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- DOI : 10.1006/bbrc.1999.0441
- ISSN : 0006-291X
- ORCIDのPut Code : 17913159
- Web of Science ID : WOS:000079615100040