C-MYC ameliorates ventricular remodeling of myocardial infarction rats via binding to the promoter of microRNA-29a-3p to facilitate TET2 expression. (15th June 2022)

• Record Type: Journal Article
• Authors: Wu, Zheng; Cheng, Shujuan; Wang, Shaoping; Li, Wenzheng; Liu, Jinghua
• Is Part Of: International journal of cardiology. Volume 357(2022)
• Page Start: 105
• Page End: 112
• Publication Date: 2022-06-15
• Subjects: Myocardial infarction -- C-MYC -- microRNA-29a-3p -- Promoter -- Ten-eleven translocation-2 -- Ventricular remodeling -- Collagen; Cardiology -- Periodicals; Electronic journals; 616.12
• DOI: 10.1016/j.ijcard.2022.01.020
• Languages: English
• ISSNs: 0167-5273

Abstract

Abstract: Background: There is increasing evidence identifying the role of c-MYC in myocardial infarction (MI). Thus, our aim was to discuss the impact of c-MYC/microRNA (miR)-29a-3p/ten-eleven translocation-2 (TET2) axis on MI. Methods: Sprague-Dawley rats received injections of recombinant adenoviruses at myocardial sites that interfered with c-MYC or miR-29a-3p expression. At 3 days after adenoviral injection, the rats were subjected to myocardial ischemia and reperfusion. Cardiac function, infarct size, cellular death, inflammatory response, oxidative stress, collagen deposition, c-MYC, TET2 and miR-29a-3p expression were analyzed. The interaction between c-MYC and miR-29a-3p as well as that between TET2 and miR-29a-3p was verified. Results: miR-29a-3p expression was enhanced while c-MYC and TET2 expression was decreased in the myocardial tissue of MI rats. Up-regulating c-MYC or down-regulating miR-29a-3p in MI rat hearts improved cardiac function and reduced infarct size and myocardial apoptotic death, restrained oxidative stress, inflammatory response, attenuated collagen deposition. c-Myc bound to the promoter of miR-29a-3p and repressed miR-29a-3p expression. TET2 was a target of miR-29a-3p. Conclusion: Our study provides evidence that c-MYC binding to the promoter of miR-29a-3p to facilitate TET2 expression has therapeutic effect on ventricular remodeling of MI rats. Highlights: Reduced c-MYC/TET2 and raised miR-29a-3p are found in myocardial tissues of MI rats. Restored c-MYC/depleted miR-29a-3p alleviates MI. Raised c-MYC/depleted miR-29a-3p suppresses apoptosis of cardiomyocytes in MI rats. There is a target relationship between miR-29a-3p and TET2. This study is essential for finding new targets for MI.