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MicroRNA‐21 mediates the rapamycin‐induced suppression of endothelial proliferation and migration
Author(s) -
Jin Chongying,
Zhao Yanbo,
Yu Lu,
Xu Shengjie,
Fu Guosheng
Publication year - 2013
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.2012.12.021
Subject(s) - downregulation and upregulation , angiogenesis , gene knockdown , sirolimus , microrna , microbiology and biotechnology , endothelial stem cell , cell growth , rhob , cancer research , chemistry , biology , signal transduction , apoptosis , gene , biochemistry , in vitro , rhoa
Rapamycin suppresses endothelial proliferation and migration, which leads to delayed re‐endothelialization in the rapamycin‐eluted stents that are used in coronary heart disease patients. Because microRNAs (miRs) play important roles in endothelial angiogenesis, we tested the hypothesis that rapamycin induces endothelial suppression, partly through pathways that involve miRs. Rapamycin treatment increased the expression of miR‐21 in HUVECs. The downregulation of miR‐21 by inhibitors abolished the negative effects of rapamycin on endothelial cell growth and mobility. RhoB was confirmed as a direct target gene of miR‐21. Knockdown of Raptor by siRNA mimicked the effects of rapamycin on miR‐21 expression. Our study provides a new explanation of the mechanism of rapamycin‐mediated inhibition of endothelial proliferation and migration.