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

Yasushi Shikata, Kenichi Shikata, Mitsuhiro Matsuda, Hikaru Sugimoto, Jun Wada, Hirofumi Makino

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

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 II effects in HMCs. In adherent cells, both FAK 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.

Original languageEnglish
Pages (from-to)234-238
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume257
Issue number1
DOIs
Publication statusPublished - Apr 2 1999

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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