Silencing of Long Noncoding RNA TUG1 Ameliorates Atherosclerosis-Induced Myocardial Injury by Upregulating microRNA-30b-3p and Downregulating Brd4.

Autor:	Li DL; Department of Cardiology, Fujian Medical University Affiliated First Quanzhou Hospital, Quanzhou, Fujian, China., Zheng BB; Department of Gastroscope, Fujian Medical University Affiliated First Quanzhou Hospital, Quanzhou, Fujian, China., Zeng X; Central laboratory, The First Affiliated Hospital Of Xiamen University, Xiamen Diabetes Institute, Xiamen, Fujian, China; and., Li J; Cardiovascular Medicine, The Affiliated Cardiovascular Hospital of Xiamen University, Xiamen, Fujian, China., Dai RZ; Department of Cardiology, Fujian Medical University Affiliated First Quanzhou Hospital, Quanzhou, Fujian, China.
Jazyk:	angličtina
Zdroj:	Journal of cardiovascular pharmacology [J Cardiovasc Pharmacol] 2023 Jan 01; Vol. 81 (1), pp. 45-54. Date of Electronic Publication: 2023 Jan 01.
DOI:	10.1097/FJC.0000000000001367
Abstrakt:	Abstract: Long noncoding RNAs and microRNAs (miRNAs) are emerging biomarkers involved in human diseases, and we focused on the roles of long noncoding RNA taurine upregulated gene 1 (TUG1) and miR-30b-3p in the related mechanisms of atherosclerosis-induced myocardial injury. ApoE-deficient mice were fed with high-fat diet to establish atherosclerotic models and then were subjected to either TUG1 downregulation or miR-30b-3p upregulation treatment. The serum myocardial enzymes, inflammatory biomarkers, pathological changes, intramyocardial macrophage infiltration, and apoptosis of cardiomyocytes in atherosclerotic mice were determined. The expression of TUG1, miR-30b-3p, and bromodomain protein 4 (Brd4) in atherosclerotic models was evaluated. Moreover, the correlations of TUG1, miR-30b-3p, and Brd4 were verified. TUG1 and Brd4 were increased while miR-30b-3p was decreased in atherosclerotic mice. The silenced TUG1 or elevated miR-30b-3p attenuated atherosclerosis-induced myocardial injury mainly by reducing serum myocardial enzyme content and inflammatory response, improving pathological changes, and preventing macrophage infiltration and cardiomyocyte apoptosis in atherosclerotic mice. Mechanistically, TUG1 could competitively bind with miR-30b-3p to prevent the degradation of its target gene Brd4. This study reveals that the silencing of TUG1 ameliorates atherosclerosis-induced myocardial injury by upregulating miR-30b-3p and downregulating Brd4, which may provide novel targets for atherosclerosis treatment. Competing Interests: The authors report no conflicts of interest. (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)
Databáze:	MEDLINE
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