lncRNA­MALAT1 promotes high glucose­induced H9C2 cardiomyocyte pyroptosis by downregulating miR­141­3p expression.

Diabetic cardiomyopathy (DCM) is caused by diabetes and can result in heart failure. Long non­coding RNAs (lncRNAs) have been demonstrated to be closely associated with DCM development. The present study aimed to investigate whether lncRNA­metastasis­associated lung adenocarcinoma transcript­1 (MALAT1) altered high glucose (HG)­induced H9C2 cardiomyocyte pyroptosis by targeting microRNA (miR)­141­3p. H9C2 cells were treated with normal glucose (NG) or HG. lncRNA­MALAT1 and miR­141­3p expression levels were determined via reverse transcription­quantitative PCR (RT­qPCR). MALAT1 and miR­141­3p knockdown and overexpression were established and confirmed via RT­qPCR. The association between MALAT1 expression and miR­141­3p expression, as well as the induction of pyroptosis and gasdermin D (GSDMD)­N expression were evaluated by performing dual luciferase reporter, TUNEL staining and immunofluorescence staining assays, respectively. Western blotting was conducted to measure the expression levels of pyroptosis­associated proteins, including apoptosis­associated speck­like protein, GSDMD­N, caspase­1, nucleotide oligomerization domain­like receptor protein 3 and GSDMD. MALAT1 mRNA expression levels were significantly increased, whereas miR­141­3p expression levels were significantly decreased in HG­treated H9C2 cells compared with the NG group. Compared with the HG group, MALAT1 overexpression significantly reduced miR­141­3p expression levels, increased the rate of TUNEL positive cells and upregulated the expression levels of pyroptosis­associated proteins. MALAT1 knockdown displayed the opposite effect on the rate of TUNEL positive cells and the expression levels of pyroptosis­associated proteins. Furthermore, the rate of TUNEL positive cells, and GSDMD­N and pyroptosis­associated protein expression levels were significantly reduced by miR­141­3p overexpression in MALAT1­overexpression H9C2 cells. The results indicated that compared with NG treatment, HG treatment increased MALAT1 expression levels and decreased miR­141­3p expression levels in H9C2 cells. Therefore, the present study suggested that lncRNA­MALAT1 targeted miR­141­3p to promote HG­induced H9C2 cardiomyocyte pyroptosis.