[Inhibition of PKC and ERK1/2 in cultured rat vascular smooth muscle cells by angiotensin-(1-7)].
The present study was undertaken to investigate the effects of angiotensin-(1-7)[Ang-(1-7)] on the proliferation and expression of protein kinase C (PKC) and extracellular regulated protein kinases (ERK1/2) of vascular smooth muscle cells (VSMCs) by techniques of Western blot, 3H-thymidine (3H-TdR) and 3H-leucine (3H-Leu) incorporation. Ang II increased VSMC DNA and protein synthesis, and promoted protein expression of PKC-zeta and ERK1/2. In contrast, Ang-(1-7) not only inhibited PKC-zeta and ERK1/2 protein content, but also decreased Ang II mediated VSMC hyperplasia, as compared with the controls (P < 0.01 or P < 0.05). These results suggest that Ang-(1-7) may inhibit VSMC proliferation by influencing protein expression of PKC-zeta and ERK1/2.
Zhong
J
J
Department of Hypertension and Endocrinology, Chongqing Institute of Hypertension, Daping Hospital, Third Military Medical University, Chongqing 400042.
Zhu
Z M
ZM
Yang
Y J
YJ
D000803:Angiotensin I / Q000494:pharmacology*; D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D019950:Mitogen-Activated Protein Kinase 1 / Q000096:biosynthesis*; D048052:Mitogen-Activated Protein Kinase 3; D020928:Mitogen-Activated Protein Kinases / Q000096:biosynthesis*; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism*; D010446:Peptide Fragments / Q000494:pharmacology*; D011493:Protein Kinase C / Q000096:biosynthesis*; D051381:Rats; D017208:Rats, Wistar
D010446:Peptide Fragments; D000803:Angiotensin I; D011493:Protein Kinase C; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D020928:Mitogen-Activated Protein Kinases; C118790:angiotensin I (1-7)