Effect of miR-155 on AngII-induced Mice Vascular Smooth Muscle Cell Phenotype Switching With its Mechanism
10.3969/j.issn.1000-3614.2017.10.019
- VernacularTitle:MiR-155对血管紧张素Ⅱ诱导小鼠主动脉血管平滑肌细胞表型转换的影响及机制研究
- Author:
wei Zi ZHANG
1
;
xia Li YANG
;
lin Jin LV
;
mei Xian WANG
;
hua Zhi YANG
;
hong Ni LU
Author Information
1. 成都军区昆明总医院 心内科
- Keywords:
RNA;
Angiotensin Ⅱ;
Muscle cells;
smooth muscle
- From:
Chinese Circulation Journal
2017;32(10):1019-1023
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To observe the effect of miR-155 on angiotensin Ⅱ (AngⅡ)-induced mice vascular smooth muscle cell (VSMC) phenotype switching with its possible mechanism. Methods: Primary cultured mice VSMCs were treated by AngⅡ at different concentrations and time periods, relevant expressions of miR-155 were examined by RT-PCR. qRT-PCR was conducted to determine miR-155 changes in Blank control group, miR-155 mimics group, miR-155 mimics negative control (NC) group, miR-155 inhibitor group and miR-155 inhibitor NC group. Western blot analysis was performed to measure the effect of miR-155 on AngⅡ-enforced ERK1/2 and mTOR signaling pathway in Blank control group, AngⅡ group, miR-155 mimics group, AngⅡ+miR-155 mimics group, miR-155 inhibitor group and AngⅡ+miR-155 inhibitor group; to detect the impact of miR-155, rapamycin (Rap) and U0126 on AngⅡ promoted VSMC phenotype switching in Blank control group, AngⅡ group, miR-155 mimics group, AngⅡ+miR-155 mimics group, AngⅡ+U0126 group and AngⅡ+Rap group, and to detect protein expressions of SM22α, α-SM-actin (contractile phenotype marker protein) and OPN (synthetic phenotype marker). Results: AngⅡ decreasing miR-155 expression was in a dose- and time-dependent manner. miR-155 could reduce the basal and AngⅡ-promoted ERK1/2, mTOR signaling pathway, while miR-155 inhibitor could elevate the above effect. Rap, U0126 and miR-155 could inhibit AngⅡ-attenuated expressions of SM22α, α-SM-actin and meanwhile inhibit AngⅡ-enforced expression of OPN. Conclusion: miR-155 could inhibit mice AngⅡ-promoted VSMC phenotype switching which might be via inhibiting the activations of mTOR and ERK1/2.
