Abstract：Objective: To investigate the effect of long-chain non-coding RNA (lncRNA) tissue differentiation-induced non-protein coding (TINCR) on the apoptosis of rat cardiomyocytes by targeting microRNA (miR)-221 expression. Methods: The cultured rat cardiomyocytes were divided into control group (normal culture), pcDNA3.1 group (transfected pcDNA3.1 empty vector) and TINCR group (transfected pcDNA3.1-TINCR overexpression vector). The expressions of TINCR and miR-221 were detected by real-time fluorescent quantitative polymerase chain reaction(PCR), the target binding relationship between TINCR and miR-221 was detected by double luciferase reporter gene assay, and the cell viability was detected by methylthiazolyldiphenyl-tetrazolium bromide (MTT), the apoptosis was detected by flow cytometry, and the expressions of B-cell lymphoma-2(Bcl-2) and Bcl-2 Associated X Protein(Bax) protein in cells were detected by Western blotting. Transfect miR-221 mimics or inhibitors into cardiomyocytes and analyze the changes of cardiomyocyte apoptosis; miR-221 mimics and pcDNA3.1-TINCR overexpression plasmid were co-transfected into cardiomyocytes to observe the effect of miR-221 on the viability and apoptosis of TINCR overexpression cardiomyocytes. Results: Compared with the control group, the expression level of miR-221, apoptosis rate and the expression level of Bax protein in TINCR group were significantly decreased, while cell survival rate and the expression level of Bcl-2 protein were significantly increased (P<0.05), but there was no statistical significance between pcDNA3.1 group and the control group (P>0.05). The results of double luciferase reporter gene showed that TINCR could bind to miR-221. Compared with the miR-NC group, the apoptosis rate and Bax protein expression level of the miR-221 group were significantly increased, and the Bcl-2 protein expression level was significantly reduced (P<0.05); and the experimental results of anti-miR-221 group are opposite. After up-regulation of miR-221 expression, the effect of TINCR overexpression on myocardial cell viability and apoptosis was significantly reversed (P<0.05).Conclusion: IncRNA TINCR can inhibit cardiomyocyte apoptosis by targeting miR-221 expression.
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2021, Vol. 27 
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