title: MicroRNA-26 was decreased in rat cardiac hypertrophy model and may be a promising therapeutic target.
abstract: MicroRNA (miR)-26 was found to be downregulated in cardiac diseases. In this study, the critical role of miR-26 in myocardial hypertrophy in both in vivo and in vitro was investigated. Sixteen male Wistar rats that underwent sham or transverse abdominal aortic constriction (TAAC) surgery were divided into control or TAAC group. Cardiomyocytes were isolated from neonatal Sprague-Dawley rats. Our study demonstrated that miR-26a/b was downregulated in both TAAC rat model and cardiomyocytes. The results of luciferase assays also suggested that glycogen synthase kinase 3β (GSK3β) may be a direct target of miR-26. The overexpression of miR-26 attenuated GSK3β expression and inhibited myocardial hypertrophy. The downregulation of miR-26 reversed these effects. Furthermore, silence of GSK3β gene phenocopied the anti-hypertrophy effects of miR-26, whereas overexpression of this protein attenuated the effects of miR-26. Taken together, these data suggest that miR-26 regulates pathological structural changes in the rat heart, which may be associated with suppression of the GSK3β signaling pathway, and implicate the potential application of miR-26 in diagnosis and therapy of cardiac hypertrophy.
authors.affiliation: *Intensive Care Unit; and †Department of Cardiology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China; ‡Guangzhou Institute of Cardiovascular Disease, Guangzhou, China; §Department of Physiology, Guangzhou Medical University, Guangzhou, China; and ¶Experimental Medicine Research Center, Guangzhou Medical University, Guangzhou, China.
authors.forename: Zhen-hui
authors.initials: ZH
authors.lastname: Zhang
authors.forename: Jiao
authors.initials: J
authors.lastname: Li
authors.forename: Ben-rong
authors.initials: BR
authors.lastname: Liu
authors.forename: Cheng-feng
authors.initials: CF
authors.lastname: Luo
authors.forename: Qi
authors.initials: Q
authors.lastname: Dong
authors.forename: Lu-ning
authors.initials: LN
authors.lastname: Zhao
authors.forename: Yun
authors.initials: Y
authors.lastname: Zhong
authors.forename: Wei-yan
authors.initials: WY
authors.lastname: Chen
authors.forename: Min-sheng
authors.initials: MS
authors.lastname: Chen
authors.forename: Shi-ming
authors.initials: SM
authors.lastname: Liu
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D006332:Cardiomegaly / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D002478:Cells, Cultured; D004195:Disease Models, Animal; D015536:Down-Regulation; D015316:Genetic Therapy; D038362:Glycogen Synthase Kinase 3 / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D057809:HEK293 Cells; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000037:antagonists & inhibitors / Q000378:metabolism*; D058990:Molecular Targeted Therapy; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D015854:Up-Regulation
chemical_list: C556274:MIRN26 microRNA, rat; D035683:MicroRNAs; D038362:Glycogen Synthase Kinase 3