In Vivo Suppression of MicroRNA-24 Prevents the Transition Toward   Decompensated Hypertrophy in Aortic-Constricted Mice

doi:10.1161/CIRCRESAHA.112.300806

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	In Vivo Suppression of MicroRNA-24 Prevents the Transition Toward Decompensated Hypertrophy in Aortic-Constricted Mice
	Li, Rong-Chang ; Tao, Jin ; Guo, Yun-Bo ; Wu, Hao-Di ; Liu, Rui-Feng ; Bai, Yan ; Lv, Zhi-Zhen ; Luo, Guan-Zheng ; Li, Lin-Lin ; Wang, Meng ; Yang, Hua-Qian ; Gao, Wei ; Han, Qi-De ; Zhang, You-Yi ; Wang, Xiu-Jie ; Xu, Ming ; Wang, Shi-Qiang
刊名	circulation research
	2013
关键词	Ca2+ signaling hypertrophic cardiomyopathy hypertrophy heart failure myocardial contraction HEART-FAILURE CARDIAC-HYPERTROPHY MYOCARDIAL-INFARCTION CELLS CALCIUM CHANNEL MUSCLE
DOI	10.1161/CIRCRESAHA.112.300806
英文摘要	Rationale: During the transition from compensated hypertrophy to heart failure, the signaling between L-type Ca2+ channels in the cell membrane/T-tubules and ryanodine receptors in the sarcoplasmic reticulum becomes defective, partially because of the decreased expression of a T-tubule-sarcoplasmic reticulum anchoring protein, junctophilin-2. MicroRNA (miR)-24, a junctophilin-2 suppressing miR, is upregulated in hypertrophied and failing cardiomyocytes. Objective: To test whether miR-24 suppression can protect the structural and functional integrity of L-type Ca2+ channel-ryanodine receptor signaling in hypertrophied cardiomyocytes. Methods and Results: In vivo silencing of miR-24 by a specific antagomir in an aorta-constricted mouse model effectively prevented the degradation of heart contraction, but not ventricular hypertrophy. Electrophysiology and confocal imaging studies showed that antagomir treatment prevented the decreases in L-type Ca2+ channel-ryanodine receptor signaling fidelity/efficiency and whole-cell Ca2+ transients. Further studies showed that antagomir treatment stabilized junctophilin-2 expression and protected the ultrastructure of T-tubule-sarcoplasmic reticulum junctions from disruption. Conclusions: MiR-24 suppression prevented the transition from compensated hypertrophy to decompensated hypertrophy, providing a potential strategy for early treatment against heart failure. (Circ Res. 2013; 112:601-605.); http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000314939400008&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701 ; Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease; SCI(E); PubMed; 35; ARTICLE; 4; 601-+; 112
语种	英语
内容类型	期刊论文
源URL	[http://ir.pku.edu.cn/handle/20.500.11897/309326]
专题	生命科学学院
推荐引用方式 GB/T 7714	Li, Rong-Chang,Tao, Jin,Guo, Yun-Bo,et al. In Vivo Suppression of MicroRNA-24 Prevents the Transition Toward Decompensated Hypertrophy in Aortic-Constricted Mice[J]. circulation research,2013.
APA	Li, Rong-Chang.,Tao, Jin.,Guo, Yun-Bo.,Wu, Hao-Di.,Liu, Rui-Feng.,...&Wang, Shi-Qiang.(2013).In Vivo Suppression of MicroRNA-24 Prevents the Transition Toward Decompensated Hypertrophy in Aortic-Constricted Mice.circulation research.
MLA	Li, Rong-Chang,et al."In Vivo Suppression of MicroRNA-24 Prevents the Transition Toward Decompensated Hypertrophy in Aortic-Constricted Mice".circulation research (2013).