Long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) is expressed in endothelial cells and involved in angiogenesis and vascular function. It was proposed that MEG3 participates in the process of endothelial progenitor cells (EPCs) functions in metabolic syndrome (MetS). In this study, the circulating EPCs number and function were decreased in MetS subjects. The MEG3 expression was expressed at a lower level and microRNA-140-5p (miR-140-5p) was expressed at a higher level in circulating EPCs of subjects with MetS. Pioglitazone reversed the alterations of EPCs function and the expression levels of MEG3 and miR-140-5p in EPCs. In bone marrow-derived EPCs exposed to palmitate, down-regulation of miR-140-5p canceled the increase of MEG3 expression level induced by Pioglitazone. Overexpression of MEG3 resulted in the down-regulation of miR-140-5p. The luciferase reporter assay and RIP assay showed that MEG3 targeted miR-140-5p. In addition, the HDAC7 expression levels were regulated by miR-140-5p and MEG3. These findings demonstrated that Pioglitazone up-regulated MEG3 expression to protect EPCs via decreasing miR-140-5p expression and increasing HDAC7 expression in MetS, which may be a novel therapeutic target for preventing and treating MetS.
Keywords: Endothelial progenitor cells; HDAC7; Metabolic syndrome; lncRNA; miR-140.
Copyright © 2016. Published by Elsevier Masson SAS.