MiR-410 inhibition induces HUVECs proliferation and represses ox-LDL-triggered apoptosis through activating STAT3.

Ox-LDL-induced endothelial cells injury has been reported to play an important role in the development of atherosclerosis (AS). MicroRNAs have been identified to regulate their target genes post-transcriptionally and they are able to participate in the various diseases, including AS. However, the role of miR-410 in ox-LDL-triggered abnormal function of endothelial cells remains to be elaborated. Hence, our current study was to find out the underlying mechanism of miR-410 in AS. Here, we observed that ox-LDL can inhibit HUVECs growth and lead to a great cell apoptosis both dose-dependently and time-dependently. Meanwhile, it was exhibited that miR-410 expression was remarkably elevated in ox-LDL-indicated HUVECs. miR-410 knockdown was able to induce cell proliferation and alleviate HUVECs apoptosis subjected to ox-LDL. Reversely, signal transducer and activator of transcription 3 (STAT3) expression was greatly decreased in ox-LDL-incubated HUVECs in a time and dose dependent manner. Additionally, these findings exhibited that STAT3 was a target of miR-410, which was validated by a dual-luciferase assay in our study. Additionally, we observed that overexpression of STAT3 rescued ox-LDL induced AS events in vitro. Taken these together, our current study implied that miR-410 silence can inhibit the ox-LDL-induced HUVECs proliferation and rescue cell apoptosis through activating STAT3 in vitro. [ABSTRACT FROM AUTHOR]