Cuiping Wang1, Xia Sun1, Zhi Qiu1, Anyong Chen2,3. 1. Department of Cardiology, Affiliated Hospital of Jining Medical University, Jining, 272000, Shandong, People's Republic of China. 2. Department of Cardiology, Affiliated Hospital of Jining Medical University, Jining, 272000, Shandong, People's Republic of China. jyfywcp@163.com. 3. Department of Clinical Laboratory, Affiliated Hospital of Jining Medical University, 89 Guhuai Road, Jining, 272000, Shandong, People's Republic of China. jyfywcp@163.com.
Abstract
OBJECTIVES: A drastic reduction in myocardial cell apoptosis plays a crucial role in the treatment/management of myocardial infarction, a major cardiovascular health challenge confronting the world, especially the Western world. Accumulating evidence indicates that the cardiotoxicity caused by the apoptotic machinery is partly regulated by miRNAs. The aim of this research is to investigate the role of miR-138-5p on hypoxia/reperfusion-induced heart injury. METHODS: The expression of miR-138-5p was determined in heart tissue from myocardial infarction patients and rats. Rats were transfection with a miR-138-5p inhibitor to silence miR-138-5p. The cardiac function of rats was detected via echocardiography. SIRT1 and PGC-1α expression in cardiac infarction was detected via quantitative Real-time PCR (qPCR) and Western blot analysis, while the TUNEL assay was used to determine myocardial apoptosis. RESULTS: Our observations showed that miR-138-5p expression was upregulated after the induction of myocardial infarction. The miR-138-5p inhibitor significantly improved cardiac function, increased the expression of SIRT1 and PGC-1α, and decreased the rate of myocardial apoptosis, whereas siRNA-SIRT1 reversed these protective effects. CONCLUSIONS: In conclusion, our study demonstrated that miR-138-5p could promote cardiac ischemia injury via inhibition of the silent information regulator 1 and peroxisome proliferator-initiated receptor gamma and coactivator 1 alpha (SIRT1-PGC-1α) axis.
OBJECTIVES: A drastic reduction in myocardial cell apoptosis plays a crucial role in the treatment/management of myocardial infarction, a major cardiovascular health challenge confronting the world, especially the Western world. Accumulating evidence indicates that the cardiotoxicity caused by the apoptotic machinery is partly regulated by miRNAs. The aim of this research is to investigate the role of miR-138-5p on hypoxia/reperfusion-induced heart injury. METHODS: The expression of miR-138-5p was determined in heart tissue from myocardial infarctionpatients and rats. Rats were transfection with a miR-138-5p inhibitor to silence miR-138-5p. The cardiac function of rats was detected via echocardiography. SIRT1 and PGC-1α expression in cardiac infarction was detected via quantitative Real-time PCR (qPCR) and Western blot analysis, while the TUNEL assay was used to determine myocardial apoptosis. RESULTS: Our observations showed that miR-138-5p expression was upregulated after the induction of myocardial infarction. The miR-138-5p inhibitor significantly improved cardiac function, increased the expression of SIRT1 and PGC-1α, and decreased the rate of myocardial apoptosis, whereas siRNA-SIRT1 reversed these protective effects. CONCLUSIONS: In conclusion, our study demonstrated that miR-138-5p could promote cardiac ischemia injury via inhibition of the silent information regulator 1 and peroxisome proliferator-initiated receptor gamma and coactivator 1 alpha (SIRT1-PGC-1α) axis.
Authors: Kojiro Nakamura; Shoichi Kageyama; Bibo Ke; Takehiro Fujii; Rebecca A Sosa; Elaine F Reed; Nakul Datta; Ali Zarrinpar; Ronald W Busuttil; Jerzy W Kupiec-Weglinski Journal: Liver Transpl Date: 2017-10 Impact factor: 5.799
Authors: Daniel P Zalewski; Karol P Ruszel; Andrzej Stępniewski; Dariusz Gałkowski; Jacek Bogucki; Łukasz Komsta; Przemysław Kołodziej; Paulina Chmiel; Tomasz Zubilewicz; Marcin Feldo; Janusz Kocki; Anna Bogucka-Kocka Journal: J Clin Med Date: 2020-06-24 Impact factor: 4.241