Premium
MiR‐20a regulates the PRKG1 gene by targeting its coding region in pulmonary arterial smooth muscle cells
Author(s) -
Zeng Yan,
Pan Yanping,
Liu Hongtai,
Kang Kang,
Wu Yike,
Hui Gang,
Peng Wenda,
Ramchandran Ramaswamy,
Raj J. Usha,
Gou Deming
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2014.10.040
Subject(s) - hypoxia (environmental) , gene , phenotype , pulmonary artery , microrna , biology , gene expression , microbiology and biotechnology , smooth muscle , pulmonary hypertension , signal transduction , vascular smooth muscle , cancer research , endocrinology , chemistry , medicine , genetics , organic chemistry , oxygen
Chronic hypoxia triggers pulmonary vascular remodeling, which is associated with de‐differentiation of pulmonary artery smooth muscle cells (PASMC). Here, we show that miR‐20a expression is up‐regulated in response to hypoxia in both mouse and human PASMC. We also observed that miR‐20a represses the protein kinase, cGMP‐dependent, type I (PRKG1) gene and we identified two crucial miR‐20a binding sites within the coding region of PRKG1. Functional studies showed that miR‐20a promotes the proliferation and migration of human PASMC, whereas it inhibits their differentiation. In summary, we provided a possible mechanism by which hypoxia results in decreased PRKG1 expression and in the phenotypic switching of PASMC.