ROCK1 and the relative signal molecules participate in proliferation of vascular smooth muscle cells induced by cyclic strain
10.16156/j.1004-7220.2017.03.01
- VernacularTitle:ROCK1及其相关信号分子参与张应变调控的血管平滑肌细胞增殖
- Author:
Li-yi WANG
1
;
Dong-ming GUO
1
;
Jing-zhi PANG
1
;
Yu-chen YANG
1
;
Bao-rong SHEN
1
;
Ying-xin QI
1
Author Information
1. Institute of Mechanobiology & Medical Engineering, School of Life Sciences And Biotechnology, Shanghai Jiao Tong University
- Publication Type:Journal Article
- Keywords:
Vascular smooth muscle cells;
Cyclic strain;
Rho-associated coiled-coil containing protein kinase 1(ROCK1);
Protein kinase
- From:
Journal of Medical Biomechanics
2017;32(3):E205-E212
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of rho-associated coiled-coil containing protein kinase 1 (ROCK1) and the relative signal molecules in sensing the mechanical stimulation from tensile strain and regulating the proliferation of vascular smooth muscle cells (VSMCs). Methods Physiological cyclic strain with magnitude of 10% and at frequency of 1.25 Hz was applied to VSMCs in vitro by using strain loading system. The proliferation level of VSMCs was analyzed by BrdU ELISA; the expression level of ROCK1, phosphorylations of protein kinase C (PKC) α/β II, protein kinase D (PKD) and extracellular regulated protein kinase (ERK) in VSMCs modulated by cyclic strain were detected with Western blotting; the expression of ROCK1 was specifically repressed by using RNA interference (RNAi). Results Compared with the static control, 10% cyclic strain significantly decreased the expression of ROCK1 and phosphorylations of PKD and ERK. The phosphorylation of PKCα/βII was decreased significantly under 10% cyclic strain for 12 h, but returned to normal level after 24 h-loading. Repressed expression of ROCK1 with RNAi significantly down-regulated VSMC proliferation, suppressed phosphorylations of PKCα/βII and PKD, but no obvious change was found in phosphorylation of ERK. Conclusions Physiological cyclic strain with magnitude of 10% may repress the phosphorylation of PKCα/βII and PKD via inhibiting the expression of ROCK1, which subsequently affect VSMC proliferation and maintain vascular hemostasis. The investigation on intracellular mechanotransduction network of VSMCs under mechanical stimulation of cyclic strain may contribute to the physiological and pathological mechanisms of cardiovascular diseases.
