RETRACTED: Long non-coding RNA TUG1 inhibits apoptosis and inflammatory response in LPS-treated H9c2 cells by down-regulation of miR-29b (Retracted article. See vol. 148, 2022)

Objective: Myocarditis is an important cause for cardiovascular morbidity and mortality in children and adults. The lncRNA taurine up-regulated gene 1 (TUG1) plays important roles in cell apoptosis and inflammation in tumor and liver injury. The present study aimed to investigate the role of TUG1 in LPS-injured H9c2 cells and explore the underlying molecular mechanism. Methods: H9c2 cells were stimulated with LPS to induce inflammatory injury. The expression of TUG1 was altered by transient transfections. Cell viability and apoptotic cell rates were detected by CCK-8 assay and flow cytometry assay, respectively. Inflammatory response was determined by detecting levels of inflammatory cytokines using qRT-PCR and ELISA. Furthermore, western blot analysis was conducted to assess the expression levels of core factors related with apoptosis and activations of NF-kappa B and JAK/STAT signaling pathways. Results: LPS exposure reduced cell viability but enhanced cell apoptosis and inflammation in H9c2 cells. Moreover, TUG1 expression was down-regulated in LPS-injured H9c2 cells. TUG1 overexpression attenuated LPS-induced injuries in H9c2 cells, evidenced by augmented cell viability, declined apoptotic cell rates and decreased levels of pro-apoptotic factors and inflammatory cytokines. Inversely, TUG1 inhibition exerted the opposite effects. More importantly, TUG1 negatively modulated the expression of miR-29b and miR-29b mimic blocked the effect of TUG1 overexpression on cell viability, apoptosis, inflammation and inactivation of NF-kappa B and JAK/STAT signaling pathways in LPS-stimulated H9c2 cells. Conclusion: This study demonstrated that TUG1 played the anti-apoptotic and anti-inflammatory roles in LPS-injured H9c2 cells via down-regulating miR-29b and inhibiting NF-kappa B and JAK/STAT pathways.