title: MicroRNA-155 inhibits angiotensin II-induced vascular smooth muscle cell proliferation.
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.
  
  
  CONCLUSIONS
  miR-155 downregulation of Ang II-induced VSMC viability identifies it as an important regulator of cell proliferation.
authors.affiliation: Department of Cardiology, Kunming General Hospital of Chengdu Military Area, China doctorlxyang@163.com.
authors.forename: Li-xia
authors.initials: LX
authors.lastname: Yang
authors.affiliation: Department of Cardiology, Kunming General Hospital of Chengdu Military Area, China.
authors.forename: Gao
authors.initials: G
authors.lastname: Liu
authors.affiliation: Department of Cardiology, Kunming General Hospital of Chengdu Military Area, China.
authors.forename: Guo-fu
authors.initials: GF
authors.lastname: Zhu
authors.affiliation: Department of Cardiology, Kunming General Hospital of Chengdu Military Area, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Liu
authors.affiliation: Department of Cardiology, Kunming General Hospital of Chengdu Military Area, China.
authors.forename: Rui-wei
authors.initials: RW
authors.lastname: Guo
authors.affiliation: Department of Cardiology, Kunming General Hospital of Chengdu Military Area, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Qi
authors.affiliation: Department of Cardiology, Kunming General Hospital of Chengdu Military Area, China.
authors.forename: Ji-hong
authors.initials: JH
authors.lastname: Zou
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D057911:Angiotensin Receptor Antagonists / Q000494:pharmacology*; D000818:Animals; D002452:Cell Count; D049109:Cell Proliferation / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D005260:Female; D051379:Mice; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000494:pharmacology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D011247:Pregnancy; D061251:Primary Cell Culture; D044140:Receptor, Angiotensin, Type 1 / Q000096:biosynthesis
chemical_list: D057911:Angiotensin Receptor Antagonists; D035683:MicroRNAs; C532623:Mirn155 microRNA, mouse; D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II
keywords: MicroRNA-155; angiotensin II; angiotensin II 1 type receptor; proliferation; vascular smooth muscle cells