Xiang-Wei Lv1, Zi-Feng He1, Pan-Pan Zhu1, Qiu-Yu Qin1, Yun-Xue Han1, Tong-Tong Xu2. 1. Department of Cardiology, Affiliated Hospital of Guilin Medical University, No.20, Lequn Road, Guilin, 541001, Guangxi Zhuang Autonomous Region, People's Republic of China. 2. Department of Cardiology, Affiliated Hospital of Guilin Medical University, No.20, Lequn Road, Guilin, 541001, Guangxi Zhuang Autonomous Region, People's Republic of China. xutongtongguilin@glmc.edu.cn.
Abstract
OBJECTIVE AND DESIGN: We aim to explore the molecular mechanism of myocardial ischemia-reperfusion injury (MIRI). METHODS: The H9C2 cells were cultured under hypoxia/reoxygenation (H/R) condition to induce myocardial injury in vitro. The expression of miR-451-3p and MAP1LC3B was detected by RT-qPCR. Dual-luciferase reporter assay and RNA pull-down assay were performed to examine the relationship between microRNA (miR)-451-3p and MAP1LC3B. CCK8 was used to test cell viability. The level of LDH and CK was evaluated via ELISA. Immunofluorescence assay and flow cytometry were applied to detect autophagy and apoptosis, respectively. Autophagy-related protein expressions were determined by western blotting. Furthermore, an in vivo rat model of MIRI was established by subjection to 30 min ischemia and subsequently 24 h reperfusion for validation of the role of miR-451-3p in regulating MIRI in vivo. RESULTS: miR-451-3p was down-regulated in MIRI, and miR-451-3p mimics transfection alleviated autophagy and apoptosis induced by MIRI. miR-451-3p could target MAP1LC3B directly. Co-transfection miR-451-3p mimics and pcDNA 3.1 MAP1LC3B curbed the protected effects of miR-451-3p mimics on MIRI. CONCLUSIONS: miR-451-3p played a protective role in MIRI via inhibiting MAP1LC3B-mediated autophagy, which may provide new molecular targets for the treatment of MIRI and further improves the clinical outcomes of heart diseases.
OBJECTIVE AND DESIGN: We aim to explore the molecular mechanism of myocardial ischemia-reperfusion injury (MIRI). METHODS: The H9C2 cells were cultured under hypoxia/reoxygenation (H/R) condition to induce myocardial injury in vitro. The expression of miR-451-3p and MAP1LC3B was detected by RT-qPCR. Dual-luciferase reporter assay and RNA pull-down assay were performed to examine the relationship between microRNA (miR)-451-3p and MAP1LC3B. CCK8 was used to test cell viability. The level of LDH and CK was evaluated via ELISA. Immunofluorescence assay and flow cytometry were applied to detect autophagy and apoptosis, respectively. Autophagy-related protein expressions were determined by western blotting. Furthermore, an in vivo rat model of MIRI was established by subjection to 30 min ischemia and subsequently 24 h reperfusion for validation of the role of miR-451-3p in regulating MIRI in vivo. RESULTS: miR-451-3p was down-regulated in MIRI, and miR-451-3p mimics transfection alleviated autophagy and apoptosis induced by MIRI. miR-451-3p could target MAP1LC3B directly. Co-transfection miR-451-3p mimics and pcDNA 3.1 MAP1LC3B curbed the protected effects of miR-451-3p mimics on MIRI. CONCLUSIONS: miR-451-3p played a protective role in MIRI via inhibiting MAP1LC3B-mediated autophagy, which may provide new molecular targets for the treatment of MIRI and further improves the clinical outcomes of heart diseases.
Authors: Sheng Shou Hu; Ling Zhi Kong; Run Lin Gao; Man Lu Zhu; Wen Wang; Yong Jun Wang; Zhao Su Wu; Wei Wei Chen; Ming Bo Liu Journal: Biomed Environ Sci Date: 2012-06 Impact factor: 3.118
Authors: Paul W Armstrong; Anthony H Gershlick; Patrick Goldstein; Robert Wilcox; Thierry Danays; Yves Lambert; Vitaly Sulimov; Fernando Rosell Ortiz; Miodrag Ostojic; Robert C Welsh; Antonio C Carvalho; John Nanas; Hans-Richard Arntz; Sigrun Halvorsen; Kurt Huber; Stefan Grajek; Claudio Fresco; Erich Bluhmki; Anne Regelin; Katleen Vandenberghe; Kris Bogaerts; Frans Van de Werf Journal: N Engl J Med Date: 2013-03-10 Impact factor: 176.079