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MicroRNA‐185 inhibits angiogenesis in human microvascular endothelial cells through targeting stromal interaction molecule 1
Author(s) -
Hou Jiayin,
Liu Liang,
Zhu Qian,
Wu Yingbiao,
Tian Bei,
Cui Li,
Liu Ying,
Li Xinming
Publication year - 2016
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10572
Subject(s) - angiogenesis , microrna , microbiology and biotechnology , stromal cell , downregulation and upregulation , gene silencing , endothelial stem cell , biology , stim1 , chemistry , cancer research , in vitro , biochemistry , gene , endoplasmic reticulum
Abstract Angiogenesis is a vital biological mechanism representing the adaptive response to a variety of pathological stimuli such as hypoxia. It is regulated by several pro‐angiogenic and anti‐angiogenic microRNAs. Studies have demonstrated an altered microRNA‐185 (miR‐185) expression in endothelial cells under hypoxic conditions; however, its role in angiogenesis has not been elucidated. We investigated the role of miR‐185 in angiogenesis and found that miR‐185 had an inhibitory effect on cell proliferation, migration, and tube formation. Stromal interaction molecule 1 (STIM1) appeared to be a direct target of miR‐185 by computational prediction; this was confirmed by luciferase reporter assay. Silencing of the STIM1 gene was found to mimic miR‐185‐mediated inhibition of angiogenesis. STIM1 overexpression eliminated the anti‐angiogenic effect of miR‐185. Our study results suggest a direct interaction between miR‐185 and STIM1 mRNA in microvascular endothelial cells. MicroRNA‐185 acted as a negative regulator of angiogenesis in microvascular endothelial cells through downregulation of the STIM1 protein.