Open AccessMicroRNA‑132 mediates proliferation and migration of pulmonary smooth muscle cells via targeting PTEN
Author(s) -
Zhenhua Zeng,
Weihua Wu,
Qi Peng,
Yun Sun,
Jianxin Liu
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.10053
Subject(s) - tensin , pten , cancer research , cell growth , microrna , biology , downregulation and upregulation , oncogene , vascular smooth muscle , cell , cell cycle , microbiology and biotechnology , chemistry , signal transduction , endocrinology , pi3k/akt/mtor pathway , smooth muscle , gene , biochemistry
Pulmonary arterial hypertension (PAH) is a severe and progressive disease characterized by the remodeling of small pulmonary arteries. The aberrant proliferation of pulmonary arterial smooth muscle cells (PASMCs) is the primary feature of PAH. MicroRNA (miR)‑132 has been demonstrated to inhibit the proliferation of vascular smooth muscle cells and repress neointimal formation. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a direct target of miR‑132 that has been revealed to be involved in the development of PAH. However, the role of miR‑132 in PAH remains unclear. The present study demonstrated that miR‑132 expression was upregulated in monocrotaline‑induced PAH rats and platelet‑derived growth factor‑induced PASMCs. In addition, treatment of PASMCs with miR‑132 mimics inhibited their proliferation, whereas miR‑132 inhibition exhibited the opposite effects. Furthermore, miR‑132 mimics promoted cell migration and maintained the PASMC contractile phenotype. Finally, the expression levels of PTEN were significantly decreased in PAH and PASMCs treated with miR‑132 mimics. Taken collectively, the data suggested that miR‑132 regulated PASMC function via PTEN and that it may be used as a potential target for the treatment of PAH.