Long noncoding RNAs (lncRNAs) are abnormally expressed in numerous diseases, and they are closely associated with cardiac diseases. However, the role of lncRNAs in lipopolysaccharide (LPS)-induced cardiotoxicity as well as the potential mechanism remain largely unclear. In the present study, IncRNA microarray assays were performed to analyze differential lncRNA expression in LPS-treated cardiomyocytes, and lncRNA FGD5-AS1 was one of the downregulated lncRNAs. H9C2 cells were treated with LPS, and the expression of lncRNA FGD5-AS1 was markedly downregulated. LncRNA FGD5 overexpression decreased the LPS-induced cardiomyocyte apoptosis and inflammation. Bioinformatics analysis and a luciferase reporter assay indicated that lncRNA FGD5-AS1 directly binds to miR-223-3p. A miR-222-3p mimic partially reversed the inhibitory effect of lncRNA FGD5-AS1 on the LPS-induced H9C2 cell apoptosis and inflammatory response. Moreover, miR-223-3p directly targeted growth arrest-specific transcript 5 (GAS5). LncRNA FGD5-AS1 regulated LPS-induced H9C2 cell inflammation and apoptosis via the miR-223-3p/GAS5 axis.
Keywords: FGD5-antisense 1; cardiomyocytes; inflammatory response; miR-223-3p.