LncRNA TINCR improves cardiac hypertrophy by regulating the miR-211-3p-VEGFB-SDF-1α-CXCR4 pathway

Abstract

AbstractCardiac hypertrophy is a common cardiovascular disease that is found worldwide and is characterized by heart enlargement, eventually resulting in heart failure. Exploring the regulatory mechanism of cardiac hypertrophy is beneficial for understanding its pathogenesis and treatment. In our study, we have showed TINCR was downregulated and miR-211–3p was upregulated in TAC- or Ang II-induced models of cardiac hypertrophy. Dual luciferase and RIP assays revealed that TINCR served as a competitive endogenous RNA (ceRNA) for miR-211–3p. Then, we observed that knockdown of miR-211–3p alleviated TAC- or Ang II-induced cardiac hypertrophy both in vivo and in vitro. Mechanistically, we demonstrated that miR-211–3p directly targeted VEGFB and thus regulated the expression of SDF-1α and CXCR4. Rescue assays further confirmed that TINCR suppressed the progression of cardiac hypertrophy by competitively binding to miR-211–3p, thereby enhancing the expression of VEGFB and activating the VEGFB-SDF-1α- CXCR4 signal. Furthermore, overexpression of TINCR suppressed TAC-induced cardiac hypertrophy in vivo by targeting miR-211–3p-VEGFB-SDF-1α- CXCR4 signalling. In conclusion, our research suggests that LncRNA TINCR improves cardiac hypertrophy by targeting miR-211–3p, thus relieving its suppressive effects on the VEGFB-SDF-1α-CXCR4 signalling axis. TINCR and miR-211–3p might act as therapeutic targets for the treatment of cardiac hypertrophy.Cardiac hypertrophy is a common cardiovascular disease worldwide, and this study may provide novel potential therapeutic targets. The authors demonstrate that TINCR improves cardiac hypertrophy by acting as a competitive endogenous RNA for miR-211-3p and thus relieving its suppressive effects on the VEGFB-SDF-1α-CXCR4 signalling axis.