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