MicroRNA-155 inhibits angiotensin II-induced vascular smooth muscle cell proliferation

作者：Yang, Li-xia^*; Liu, Gao; Zhu, Guo-fu; Liu, Hong; Guo, Rui-wei; Qi, Feng; Zou, Ji-hong

来源：Journal of the Renin-Angiotensin-Aldosterone System, 2014, 15(2): 109-116.

DOI：10.1177/1470320313503693

• MicroRNA-155
• angiotensin II
• angiotensin II 1 type receptor
• vascular smooth muscle cells
• proliferation

Background: MicroRNA-155 (miR-155) is a multifunctional signal microRNA that participates in a variety of cardiovascular diseases and is involved in physiological and pathological processes in different cell types.
Objective: The objective of this article is to examine the effect of miR-155 on angiotensin II (Ang II)-induced primary mice vascular smooth muscle cell (VSMC) proliferation.
Methods: Primary cultured VSMCs from the aorta of C57/BL6 mice were incubated with Ang II and miR-155. Cells were counted using CCK-8 and EdU, and flow cytometric analysis of cell cycle progression was performed. Angiotensin II 1 type receptor (AT1R) gene and protein expression were measured by real-time polymerase chain reaction and Western blotting.
Results: 1) Ang II increased the viability of VSMCs in a dose-and time-dependent manner. 2) miR-155 opposed the Ang II-induced increase in VSMC viability. 3) miR-155 inhibited Ang II-induced proliferation of VSMCs. 4) miR-155 increased the number of VSMCs in the G1 phase compared to G2 and M cell cycle phases. 5) miR-155 decreased ATR1 gene and protein expression.
Conclusion: miR-155 downregulation of Ang II-induced VSMC viability identifies it as an important regulator of cell proliferation.

• 出版日期2014-6
• 单位成都军区昆明总医院