LncRNA TUG1 contributes to cardiac hypertrophy via regulating miR-29b-3p.

Abstract

Cardiac hypertrophy with maladjusted cardiac remodeling is the leading cause of heart failure. In the past decades, long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been proved to exert multiple functions in cellular biological behaviors; however, their role in cardiac hypertrophy remains largely unclear. Presently, we first obtained hypertrophic H9c2 cells by treating with angiotensin II (Ang II) and uncovered upregulation of lncRNA taurine upregulated gene 1 (TUG1) in such H9c2 cells. Then, we demonstrated that silencing TUG1 attenuated Ang II-induced cardiac hypertrophy. Besides, a strong interactivity of TUG1 with miR-29b-3p at the putative sites was validated, suggesting that TUG1 was an endogenous sponge of miR-29b-3p in H9c2 cells. Additionally, the expression of miR-29b-3p was strikingly reduced by TUG1 upregulation and also inhibited under Ang II treatment, whereas it was restored after silencing TUG1 in hypertrophic cells. Also, we proved miR-29b-3p as a negative regulator in cardiac hypertrophy. Finally, miR-29b-3p inhibition abolished the anti-hypertrophy effect of TUG1 depletion in Ang II-treated H9c2 cells. Collectively, our findings confirmed that TUG1 functioned as a positive modulator of cardiac hypertrophy via sponging miR-29b-3p, indicating that TUG1 might serve as a potential target for the treatment of cardiac hypertrophy and even heart failure.