Knockdown of long noncoding RNA GAS5 protects human cardiomyocyte-like AC16 cells against high glucose-induced inflammation by inhibiting miR-21-5p-mediated TLR4/NF-κB signaling.

Abstract

Diabetic cardiomyopathy (DCM) is a common cause of disability and death among diabetic patients. In this study, we aimed to identify the functional role of long noncoding RNA GAS5 in human cardiomyocyte-like AC16 cells under high glucose (HG) condition. The results showed that HG treatment induced damage in AC16 cells by decreasing cell viability and increasing cell apoptosis. We also found that HG increased GAS5 expression in AC16 cells and knockdown of GAS5 protected AC16 cells from HG-induced injury. Furthermore, we confirmed that GAS5 could competitively bind with miR-21-5p and miR-21-5p inhibition alleviated the beneficial effects of GAS5 knockdown against HG stimulation. TLR4 was identified as a target of miR-21-5p in AC16 cells, and GAS5 knockdown alleviated HG-induced inflammation partly by inhibiting miR-21-5p-mediated TLR4/NF-κB signaling. Our results suggested that GAS5/miR-21-5p axis may serve as a candidate therapeutic target for DCM.