Long non-coding RNA DLX6-AS1 accelerates lipopolysaccharides-induced human AC16 cardiomyocytes apoptosis by regulating miR-497/CaSR axis

Abstract

Long non-coding RNAs (lncRNAs) are a kind of non-coding RNAs which may play vital roles in bacterial infection induced cardiomyocytes injury. We aim to investigated the roles of lncRNA DLX6-AS1 in LPS-induced human AC16 cardiomyocytes apoptosis and investigate the corresponding mechanisms in this study. The expression of DLX6-AS1 in LPS-injured human AC16 cardiomyocytes was detected by RT-PCR. The functions of DLX6-AS1 and miR-497 on AC16 cells apoptosis and viability were studied using flow cytometry, Caspase 3 activity analysis, and CCK8 assay. DLX6-AS1 was upregulated in LPS-induced human AC16 cardiomyocytes and the high-level DLX6-AS1 accelerated apoptosis and restrained viability of LPS-injured AC16 cells. MiR-497 was a target of DLX6-AS1. DLX6-AS1 mediates apoptosis of LPS-induced AC16 cardiomyocytes injury via miR-497. DLX6-AS1/miR-497 regulated endoplasmic reticulum (ER) stress‑associated apoptosis via regulating Calcium-sensing Receptor (CaSR). DLX6-AS1 was upregulated in LPS-induced human AC16 cardiomyocytes and involved in the LPS-induced AC16 cells apoptosis via facilitating ER stress by modulating miR-497/CaSR signaling pathway.