LncRNA TTTY15 knockdown alleviates H2O2-stimulated myocardial cell injury by regulating the miR-98-5p/CRP pathway.

Acute myocardial infarction (AMI) can lead to myocardial injury, and long non-coding RNA (lncRNA) has been found to play an important regulatory role in the process of myocardial injury. However, the role and potential mechanisms of lncRNA testis-specific transcript Y-linked 15 (TTTY15) in AMI-induced myocardial injury has not been fully elucidated. Hydrogen peroxide (H2O2)-induced AMI cell model was built and AMI mice model were constructed. Relative expression levels of TTTY15, miR-98-5p and C-reactive protein (CRP) were determined by quantitative real-time PCR (qRT-PCR). Cell counting kit 8 (CCK8) assay, flow cytometry and enzyme-linked immunosorbent assay (ELISA) were employed to assess cell viability, apoptosis, inflammatory response and oxidative stress. Western blot (WB) analysis was used to assess the protein expression levels. The mechanism of TTTY15 was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Our results revealed that TTTY15 was upregulated and miR-98-5p was downregulated in AMI patients and H2O2-stimulated myocardial cells. Knockdown of TTTY15 could alleviate H2O2-stimulated myocardial cell injury in vitro and AMI progression in vivo. Bioinformatics analysis and the rescue experiments confirmed that TTTY15 positively regulated H2O2-induced myocardial cell injury via regulating CRP by sponging miR-98-5p. Our research proposed that lncRNA TTTY15 promoted myocardial cell injury by regulating the miR-98-5p/CRP axis, suggesting that TTTY15 might be a potential target for alleviating AMI-caused myocardial cell injury.