LAUSR

ABSTRACT Myocardial infarction (MI) is a leading cause of heart failure (HF) all over the world. Long non-coding RNAs (lncRNAs) have been reported to be associated with the development of MI. Here, we aimed to explore the effects of lncRNA small nuclear RNA host gene 7 (SNHG7) on MI, and the possible mechanism. In this study, MI model was established by ligating the left anterior descending coronary artery of mice. Cardiac fibroblasts (CFs) derived from neonatal mice were activated by angiotensin II (Ang-II) treatment. The expression of SNHG7 and miR-455-3p was examined by quantitative real-time PCR (qRT-PCR), and protein levels of platelet activating factor receptor (PTAFR) and fibrosis-related proteins were analyzed by Western blot assay. Cell apoptosis of CFs was monitored by Flow cytometry. Enzyme-linked immunosorbent assay (ELISA) was performed to evaluate inflammatory response in CFs. Moreover, dual-luciferase reporter assay was employed to confirm the target relationship between miR-455-3p and SNHG7 or PTAFR. LncRNA SNHG7 and PTAFR were upregulated, while miR-455-3p was downregulated in cardiac tissues of MI mice and Ang-II-induced CFs. SNHG7 depletion or miR-455-3p overexpression attenuated Ang-II-induced apoptosis, fibrosis and inflammation in CFs, which was severally weakened by miR-455-3p inhibition or PTAFR upregulation. LncRNA SNHG7 targeted miR-455-3p, and PTAFR was a target of miR-455-3p. LncRNA SNHG7 depletion exerted protective roles in apoptosis, fibrosis and inflammation in Ang-II-induced CFs by regulating miR-455-3p/PTAFR axis, providing a potential molecular target for MI therapy.