Involvement of Rho and tyrosine kinase in angiotensin II-induced actin reorganization in mesothelial cells.
We investigated the role of angiotensin II type 1 (AT(1)) receptors in angiotensin II-induced actin reorganization and the signaling pathways of the response in pleural mesothelial cells. The effects of angiotensin II on actin reorganization in pleural mesothelial cells were evaluated by dual fluorescence labeling of filamentous (F) and monomeric (G) actin with fluorescein isothiocyanate (FITC)-labeled phalloidin and Texas Red-labeled DNase I, respectively. Angiotensin II (10 microM) induced actin reorganization in the presence and the absence of extracellular Ca(2+). An angiotensin AT(1) receptor antagonist ([Sar(1),Ile(8)]angiotensin II) inhibited angiotensin II-induced actin reorganization. Pretreatment with C3 exoenzyme or tyrosine kinase inhibitors significantly reduced angiotensin II-induced actin reorganization. However, pertussis toxin, phosphatidylinositol-3-kinase and protein kinase C inhibitors had no effect on these responses. These results suggest that angiotensin II-induced actin reorganization in pleural mesothelial cells is extremely dependent on the angiotensin AT(1) receptor coupled with pertussis toxin-insensitive heterotrimeric G proteins, Rho GTPases and tyrosine phosphorylation pathways.
Kuwahara
Masayoshi
M
Department of Comparative Pathophysiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, 113-8657, Tokyo, Japan. akuwam@mail.ecc.u-tokyo.ac.jp
Kuwahara
Maki
M
D015059:1-Sarcosine-8-Isoleucine Angiotensin II / Q000494:pharmacology; D036002:ADP Ribose Transferases / Q000494:pharmacology; D000199:Actins / Q000187:drug effects* / Q000378:metabolism; D000730:Androstadienes / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology*; D057911:Angiotensin Receptor Antagonists; D000818:Animals; D001905:Botulinum Toxins; D002460:Cell Line; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D019833:Genistein / Q000494:pharmacology; D007211:Indoles / Q000494:pharmacology; D008301:Maleimides / Q000494:pharmacology; D018613:Microscopy, Confocal; D037342:Pertussis Toxin; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D044140:Receptor, Angiotensin, Type 1; D013997:Time Factors; D010566:Virulence Factors, Bordetella / Q000494:pharmacology; D000077191:Wortmannin; D020741:rho GTP-Binding Proteins / Q000378:metabolism*
D000199:Actins; D000730:Androstadienes; D057911:Angiotensin Receptor Antagonists; D004791:Enzyme Inhibitors; D007211:Indoles; D008301:Maleimides; D044140:Receptor, Angiotensin, Type 1; D010566:Virulence Factors, Bordetella; D000804:Angiotensin II; D015059:1-Sarcosine-8-Isoleucine Angiotensin II; D019833:Genistein; D036002:ADP Ribose Transferases; C063007:exoenzyme C3, Clostridium botulinum; D037342:Pertussis Toxin; D011505:Protein-Tyrosine Kinases; D011493:Protein Kinase C; D001905:Botulinum Toxins; D020741:rho GTP-Binding Proteins; C070515:bisindolylmaleimide I; D000077191:Wortmannin