Long Noncoding RNA Small Nuclear RNA Host Gene 7 Knockdown Protects Mouse Cardiac Fibroblasts Against Myocardial Infarction by Regulating miR-455-3p/Platelet-Activating Factor Receptor Axis.

ABSTRACT: Myocardial infarction (MI) is a leading cause of heart failure all over the world. Long noncoding RNAs have been reported to be associated with the development of MI. In this article, we aimed to explore the effects of long noncoding RNA small nuclear RNA host gene 7 (SNHG7) on MI and the possible mechanism. In this study, an 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 polymerase chain reaction, 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 was performed to evaluate inflammatory responses in CFs. Moreover, dual-luciferase reporter assay was used to confirm the target relationship between miR-455-3p and SNHG7 or PTAFR. LncRNA SNHG7 and PTAFR were upregulated, whereas miR-455-3p was downregulated in cardiac tissues of mice with MI 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.