LncRNA TINCR Suppressed Bnip3 Expression to Improve Cardiomyocyte Viability under High Glucose Conditions

Abstract

Background: The viability of cardiomyocytes is crucial for maintaining normal myocardial function. Studies have suggested that lncRNA terminal differentiation-induced non-protein coding RNA (TINCR), a long non-coding RNA, played a protective role against cardiac hypertrophy, which was associated with reduced cardiomyocyte viability, as observed in diabetic cardiomyopathy. This study aimed to investigate the mechanisms and role of lncRNA TINCR in cardiomyocyte viability under high glucose conditions. Methods: A total of 180 individuals, including 60 diabetic cardiomyopathy patients, 60 diabetic patients without complications and 60 healthy controls, were enrolled. RNA was extracted from the blood samples using Trizol reagent, followed by cDNA synthesis of TINCR and Bnip3 (BCL2/adenovirus E1B 19 kDa protein-interacting protein 3). Amplification of the cDNA was carried out through real-time quantitative PCR. AC16 (human cardiomyocyte cell line) was cultured in Dulbeccos modified Eagles medium (DMEM) and was transfected with a TINCR expression vector. The viability of the cells and Bnip3 expression level of proteins were determined through 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyl-2H-Tetrazolium Bromide (MTT) assay and western blot analysis, respectively. The optical density (OD) was measured using a spectrophotometer, and cellular apoptosis was determined by flow cytometry. SPSS19.0 was used for statistical analysis. Results: We found that TINCR was downregulated and Bnip3 was upregulated in diabetic cardiomyopathy patients. Furthermore, high glucose treatment of the cells did not significantly affect TINCR expression in cardiomyocytes. Moreover, there was a significant negative correlation between Bnip3 mRNA expression and TINCR in diabetic cardiomyopathy patients, but not in other two groups. We found that overexpression of TINCR under high glucose conditions inhibited Bnip3 expression, suppressed cell apoptosis and improved cardiomyocyte viability. Conclusions: LncRNA TINCR suppressed Bnip3 expression, thus enhancing cardiomyocyte viability under high glucose conditions in diabetic cardiomyopathy.