Tian-Ping Chen1, Nai-Ju Zhang2, Hong-Ju Wang2, Si-Gan Hu2, Xu Geng2. 1. Department of Cardiology, the First Affiliated Hospital of Bengbu Medical College, No. 287, Changhuai Road, Longzi Lake District, Bengbu city, 233003, Anhui province, China. ra3330@163.com. 2. Department of Cardiology, the First Affiliated Hospital of Bengbu Medical College, No. 287, Changhuai Road, Longzi Lake District, Bengbu city, 233003, Anhui province, China.
Abstract
BACKGROUND: Studies have found that circular RNAs (circRNAs) play key roles in cardiovascular diseases. However, the function of circROBO2 in acute myocardial infarction (AMI) is unclear. This study aimed to investigate the pathogenesis of circROBO2 in AMI. METHODS: qRT-PCR and Western blot were used to determine the expression levels of circROBO2, miR-1184, and TRADD in AMI and sham-operated mouse models at mRNA and protein level, respectively. The relationship among miR-1184, circROBO2 and TRADD was evaluated by RNA immunoprecipitation (RIP) analysis and luciferase reporter gene analysis. The roles of circROBO2, miR-1184, and TRADD in myocardial cell apoptosis were evaluated using flow cytometry. Ultrasound echocardiography, serum creatine kinase MB (CK-MB) and lactate dehydrogenase (LDH), myocardial infarction area, and myocardial cell apoptosis were measured to examine the effects of circROBO2 on myocardial injury. RESULTS: The expression levels of miR-1184 were significantly reduced, and the expression levels of circROBO2 and TRADD were significantly increased in MI group. CircROBO2 acted as a sponge for miR-1184 by upregulating the expression of TRADD. In addition, overexpression of miR-1184 enhanced the protective effect of knockdown of circROBO2 by partially inhibiting the expression of TRADD in vivo and in vitro. CONCLUSION: Knockdown of circROBO2 reduced the apoptosis of cardiomyocytes by increasing the expression levels of miR-1184, which in turn decreased the expression levels of TRADD in the myocardium post-MI.
BACKGROUND: Studies have found that circular RNAs (circRNAs) play key roles in cardiovascular diseases. However, the function of circROBO2 in acute myocardial infarction (AMI) is unclear. This study aimed to investigate the pathogenesis of circROBO2 in AMI. METHODS: qRT-PCR and Western blot were used to determine the expression levels of circROBO2, miR-1184, and TRADD in AMI and sham-operated mouse models at mRNA and protein level, respectively. The relationship among miR-1184, circROBO2 and TRADD was evaluated by RNA immunoprecipitation (RIP) analysis and luciferase reporter gene analysis. The roles of circROBO2, miR-1184, and TRADD in myocardial cell apoptosis were evaluated using flow cytometry. Ultrasound echocardiography, serum creatine kinase MB (CK-MB) and lactate dehydrogenase (LDH), myocardial infarction area, and myocardial cell apoptosis were measured to examine the effects of circROBO2 on myocardial injury. RESULTS: The expression levels of miR-1184 were significantly reduced, and the expression levels of circROBO2 and TRADD were significantly increased in MI group. CircROBO2 acted as a sponge for miR-1184 by upregulating the expression of TRADD. In addition, overexpression of miR-1184 enhanced the protective effect of knockdown of circROBO2 by partially inhibiting the expression of TRADD in vivo and in vitro. CONCLUSION: Knockdown of circROBO2 reduced the apoptosis of cardiomyocytes by increasing the expression levels of miR-1184, which in turn decreased the expression levels of TRADD in the myocardium post-MI.
Authors: Maarten F Corsten; Robert Dennert; Sylvia Jochems; Tatiana Kuznetsova; Yvan Devaux; Leon Hofstra; Daniel R Wagner; Jan A Staessen; Stephane Heymans; Blanche Schroen Journal: Circ Cardiovasc Genet Date: 2010-10-04
Authors: D G Jackson-Bernitsas; H Ichikawa; Y Takada; J N Myers; X L Lin; B G Darnay; M M Chaturvedi; B B Aggarwal Journal: Oncogene Date: 2006-09-04 Impact factor: 9.867
Authors: F Lin; G A Zhao; Z G Chen; X H Wang; F H Lü; Y C Zhang; R Y Cai; W Q Liang; J H Li; M Li; G H Zhang; Y M Yang Journal: Zhonghua Yi Xue Za Zhi Date: 2018-03-20