A Dysregulated MicroRNA-26a/EphA2 Axis Impairs Endothelial Progenitor Cell Function via the p38 MAPK/VEGF Pathway
Author(s) -
Keqiang Zuo,
Kangkang Zhi,
Xiaoping Zhang,
Chenghui Lu,
Shi Wang,
Maoquan Li,
Bin He
Publication year - 2015
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000369713
Subject(s) - gene knockdown , progenitor cell , microrna , cancer research , mapk/erk pathway , downregulation and upregulation , endothelial progenitor cell , eph receptor a2 , viability assay , p38 mitogen activated protein kinases , medicine , blot , mtt assay , cell , biology , signal transduction , microbiology and biotechnology , stem cell , cell culture , biochemistry , genetics , gene , receptor tyrosine kinase
Dysfunction of circulating endothelial progenitor cells (EPCs) is associated with the onset of cardiovascular disorders. Circulating microRNAs (miRNAs) have been recognized as novel biomarkers and potential therapeutic targets. Here, we examined the role of miR-26a overexpression in atherosclerosis and explored the underlying mechanisms.
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