Li-xia Yang1, Gao Liu2, Guo-fu Zhu2, Hong Liu2, Rui-wei Guo2, Feng Qi2, Ji-hong Zou2. 1. Department of Cardiology, Kunming General Hospital of Chengdu Military Area, China doctorlxyang@163.com. 2. Department of Cardiology, Kunming General Hospital of Chengdu Military Area, China.
Abstract
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.
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.
Authors: Claudio de Lucia; Klara Komici; Giulia Borghetti; Grazia Daniela Femminella; Leonardo Bencivenga; Alessandro Cannavo; Graziamaria Corbi; Nicola Ferrara; Steven R Houser; Walter J Koch; Giuseppe Rengo Journal: Front Med (Lausanne) Date: 2017-06-12