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学科主题: 临床医学
题名:
In Vivo Suppression of MicroRNA-24 Prevents the Transition Toward Decompensated Hypertrophy in Aortic-Constricted Mice
作者: Li, Rong-Chang1,2; Tao, Jin1,2; Guo, Yun-Bo1,2; Wu, Hao-Di1,2; Liu, Rui-Feng1,2; Bai, Yan1,2; Lv, Zhi-Zhen1,2; Luo, Guan-Zheng3; Li, Lin-Lin1,2; Wang, Meng3; Yang, Hua-Qian1,2; Gao, Wei1,2; Han, Qi-De1,2; Zhang, You-Yi1,2; Wang, Xiu-Jie3; Xu, Ming1,2; Wang, Shi-Qiang1,2
关键词: Ca2+ signaling ; hypertrophic cardiomyopathy ; hypertrophy ; heart failure ; myocardial contraction
刊名: CIRCULATION RESEARCH
发表日期: 2013-02-15
DOI: 10.1161/CIRCRESAHA.112.300806
卷: 112, 期:4, 页:601-+
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cardiac & Cardiovascular Systems ; Hematology ; Peripheral Vascular Disease
研究领域[WOS]: Cardiovascular System & Cardiology ; Hematology
关键词[WOS]: HEART-FAILURE ; CARDIAC-HYPERTROPHY ; MYOCARDIAL-INFARCTION ; CELLS ; CALCIUM ; CHANNEL ; MUSCLE
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.)

语种: 英语
所属项目编号: 2011CB809101 ; 81070196 ; 30730013 ; 81030001 ; 81121061 ; XDA01020105 ; R01 TW007269
项目资助者: 973 Program of China ; National Natural Science Foundation of China ; Chinese Academy of Sciences ; Program for New Century Excellent Talents in University ; Beijing Talents Foundation ; NIH, USA
WOS记录号: WOS:000314939400008
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/61541
Appears in Collections:北京大学第三临床医学院_期刊论文

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作者单位: 1.Peking Univ, Coll Life Sci, Beijing 100871, Peoples R China
2.Peking Univ, Hosp 3, Key Lab Cardiovasc Mol Biol & Regulatory Peptides, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100871, Peoples R China
3.Chinese Acad Sci, Key Lab Genet Network Biol, Inst Genet & Dev Biol, Beijing, Peoples R China

Recommended Citation:
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,2013,112(4):601-+.
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