Long noncoding RNA MEG3 suppressed endothelial cell proliferation and migration through regulating miR-21.

Long non-coding RNAs (lncRNAs) act critical roles in many biological processes, including cell proliferation, apoptosis, development, invasion and migration. LncRNA maternally expressed gene 3 (MEG3) is found to be downregulated in several tumors; however, its role in the atherosclerosis is still unknown. In the present study, we demonstrated that MEG3 expression level was downregulated in the coronary artery disease (CAD) tissues compared to in the control tissues. We also showed that TNF-α enhanced EC cell proliferation. In addition, the expression of MEG3 was increased in EC after treated with TNF-α. Overexpression of MEG3 suppressed EC cell proliferation and inhibited the expression of cyclin D1, ki-67 and PCNA. Elevated expression of MEG3 suppressed the type I collagen, type V collagen and proteoglycan expression. In addition, we showed that elevated expression of MEG3 suppressed the miR-21 expression in the EC and promoted the expression of RhoB and PTEN, which were the direct target genes of miR-21. We demonstrated that miR-21 expression level was upregulated in the CAD tissues compared to in the control tissues. Moreover, miR-21 expression was reversely correlated with MEG3 expression in the CAD tissues. Overexpression of MEG3 suppressed EC cell proliferation and type I collagen, type V collagen and proteoglycan expression through inhibiting miR-21 expression. These results suggested that MEG3 played a critical role in regulating EC proliferation and type I collagen, type V collagen and proteoglycan expression partly through suppressing miR-21 expression.