LncRNA LINC00961 regulates endothelial‑mesenchymal transition via the PTEN‑PI3K‑AKT pathway.

Abstract

The long noncoding RNA LINC00961 plays a crucial role in cancer and cardiovascular diseases. In the present study, the role and underlying mechanism of LINC00961 in endothelial-mesenchymal transition (EndMT) induced by transforming growth factor beta (TGF-β), was investigated. Human cardiac microvascular endothelial cells were transfected with LV-LINC00961 or short hairpin LINC00961 plasmids to overexpress or knock down LINC00961 in the cells, respectively. The cells were then exposed to TGF-β in serum-free medium for 48 h to induce EndMT. Flow cytometric analysis, Cell Counting Kit-8 assay and immunofluorescence staining were performed to examine the cell apoptosis rate, assess cell viability, and identify CD31+/α-SMA+ double-positive cells, respectively. Western blotting and reverse transcription- quantitative polymerase chain reaction were used to evaluate protein and mRNA expression, respectively. Injury to endothelial cells and EndMT was induced by TGF-β in a time-dependent manner. LINC00961 overexpression promoted injury and EndMT, whereas LINC00961 knockdown had the opposite effects. Knockdown of LINC00961 attenuated EndMT and injury to endothelial cells induced by TGF-β via the PTEN-PI3K-AKT pathway. Inhibition of LINC00961 expression may prevent the occurrence of EndMT-related cardiovascular diseases, such as myocardial fibrosis and heart failure. Therefore, LINC00961 shows potential as a therapeutic target for cardiovascular diseases.