MicroRNA-103/107 Regulate Programmed Necrosis and Myocardial Ischemia/Reperfusion Injury Through Targeting FADD

• DOI: 10.1161/circresaha.117.305781
• Publication Date: 2015-06-03T03:27:05Z
• Authors: Jian-Xun Wang; Xiao-Jie Zhang; Qian Li; Kun Wang; Yin Wang; Jian-Qin Jiao; Chang Feng; Sun Teng; Lu-Yu Zhou; Ying Gong; Zhi-Xia Zhou; Jia Liu; Jian-Ling Wang; Pei-feng Li
• Keywords: FADD; RIPK1; Caspase 8

Necrosis is one of the main forms cardiomyocyte death in heart disease. Recent studies have demonstrated that certain types necrosis are regulated and programmed dependent on activation receptor-interacting serine/threonine-protein kinase (RIPK) 1 3 which may be negatively by Fas-associated protein with domain (FADD). In addition, microRNAs long noncoding RNAs been shown to play important roles various biological processes recently.The purpose this study was test hypothesis microRNA-103/107 H19 can participate regulation RIPK1- RIPK3-dependent fetal cardiomyocyte-derived H9c2 cells myocardial infarction through targeting FADD.Our results show FADD participates H2O2-induced influencing formation RIPK1 RIPK3 complexes cells. We further demonstrate miR-103/107 target directly. Knockdown antagonizes cellular model also a mouse ischemia/reperfusion model. The miR-103/107-FADD pathway does not tumor factor-α-induced necrosis. exploring molecular mechanism regulated, we RNA directly binds regulates expression necrosis.Our reveal novel model, composed H19, miR-103/107, FADD. Modulation their levels provide new approach for preventing