Shear stress and vascular smooth muscle cells modulate the proliferation of endothelial cells via TGFβ1 and p-Akt pathways
- VernacularTitle:切应力与血管平滑肌细胞对内皮细胞增殖的影响及TGFβ1与p-Akt信号通路在其中的作用
- Author:
Xiao hua JIANG
1
;
Qing ping YAO
1
;
Jun JIANG
1
;
Su ying JI
1
;
Ying xin QI
1
;
Zong lai JIANG
1
Author Information
1. Institute of Mechanobiology & Medical Engineering, Shanghai Jiao Tong University
- Publication Type:Journal Article
- Keywords:
Shear stress;
Vascular smooth muscle cells;
Endothelial cells;
Cell proliferation;
Cell culture
- From:
Journal of Medical Biomechanics
2010;25(5):E316-E320
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of shear stress and vascular smooth muscle cells (VSMCs) on the proliferation of endothelial cells (ECs) and the molecular mechanism involved in. Method Using parallel-plate flow chamber system, normal shear stress of 15 dyn/cm2(1 dyn=10-5 N) was applied to ECs cultured singly and co cultured with VSMCs respectively. Then, the expression of PCNA, a molecule representing cell proliferation ability, and phosphorylation of Akt were analyzed by Western blotting in order to investigate the roles of shear stress and VSMCs in EC proliferation. Under the static condition, the expressions of PCNA and p-Akt were analyzed in ECs co-cultured with VSMCs with and without physical contact. And then TGFβ1 neutralizing antibody was employed to demonstrate the contribution of TGFβ1 in VSMCs induced EC proliferation. Results Normal shear stress decreased EC proliferation and Akt phosphorylation. VSMCs increased EC proliferation and Akt phosphorylation in both co-culture conditions with and without physical contact. Normal shear stress partly reversed the increase of proliferation and Akt phosphorylation in ECs with physical contact to VSMCs, and TGFβ1 neutralizing antibody exerted the similar effects in ECs without physical contact to VSMCs. Conclusions Normal shear stress is a protective factor with its inhibitory effect on EC proliferation. VSMCs induced EC proliferation via TGFβ1 and p Akt pathways by paracrine model.
