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学科主题: 临床医学
题名:
TNNI3K, a Cardiac-Specific Kinase, Promotes Physiological Cardiac Hypertrophy in Transgenic Mice
作者: Wang, Xiaojian1,2; Wang, Jizheng1,2; Su, Ming1,2; Wang, Changxin1,2; Chen, Jingzhou1,2; Wang, Hu1,2; Song, Lei2,3; Zou, Yubao2,3; Zhang, Lianfeng4,5; Zhang, Youyi6; Hui, Rutai1,2
刊名: PLOS ONE
发表日期: 2013-03-05
DOI: 10.1371/journal.pone.0058570
卷: 8, 期:3
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Multidisciplinary Sciences
研究领域[WOS]: Science & Technology - Other Topics
关键词[WOS]: TROPONIN-I PHOSPHORYLATION ; PROTEIN-C PHOSPHORYLATION ; HUMAN HEART-MUSCLE ; FAILURE ; BINDING ; OVEREXPRESSION ; CARDIOMYOCYTES ; EXPRESSION ; GENE
英文摘要:

Purpose: Protein kinase plays an essential role in controlling cardiac growth and hypertrophic remodeling. The cardiac troponin I-interacting kinase (TNNI3K), a novel cardiac specific kinase, is associated with cardiomyocyte hypertrophy. However, the precise function of TNNI3K in regulating cardiac remodeling has remained controversial.

Methods and Results: In a rat model of cardiac hypertrophy generated by transverse aortic constriction, myocardial TNNI3K expression was significantly increased by 1.62 folds (P<0.05) after constriction for 15 days. To investigate the role of TNNI3K in cardiac hypertrophy, we generated transgenic mouse lines with overexpression of human TNNI3K specifically in the heart. At the age of 3 months, the high-copy-number TNNI3K transgenic mice demonstrated a phenotype of concentric hypertrophy with increased heart weight normalized to body weight (1.31 fold, P<0.01). Echocardiography and non-invasive hemodynamic assessments showed enhanced cardiac function. No necrosis or myocyte disarray was observed in the heart of TNNI3K transgenic mice. This concentric hypertrophy maintained up to 12 months of age without cardiac dysfunction. The phospho amino acid analysis revealed that TNNI3K is a protein-tyrosine kinase. The yeast two-hybr !E cipitation assay identified cTnI as a target for TNNI3K. Moreover, TNNI3K overexpression induced cTnI phosphorylation at Ser22/Ser23 in vivo and in vitro, suggesting that TNNI3K is a novel upstream regulator for cTnI phosphorylation.

Conclusion: TNNI3K promotes a concentric hypertrophy with enhancement of cardiac function via regulating the phosphorylation of cTnI. TNNI3K could be a potential therapeutic target for preventing from heart failure.

语种: 英语
所属项目编号: 2007DFC30340 ; 2009ZX09501-026 ; 30840041 ; 30700322
项目资助者: Ministry of Science and Technology of China ; National Science and Technology Major Projects ; National Natural Science Foundation of China
WOS记录号: WOS:000315637900153
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/61533
Appears in Collections:北京大学第三临床医学院_心血管内科_期刊论文

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作者单位: 1.Chinese Acad Med Sci, Peking Union Med Coll, FuWai Hosp, Sinogerman Lab Mol Med,State Key Lab Cardiovasc D, Beijing 100730, Peoples R China
2.Chinese Acad Med Sci, Peking Union Med Coll, Cardiovasc Inst, Beijing 100730, Peoples R China
3.Chinese Acad Med Sci, Peking Union Med Coll, FuWai Hosp, Dept Cardiol,State Key Lab Cardiovasc Dis, Beijing 100730, Peoples R China
4.Chinese Acad Med Sci, Inst Lab Anim Sci, Minist Hlth, Key Lab Human Dis Comparat Med, Beijing 100730, Peoples R China
5.Peking Union Med Coll, Comparat Med Ctr, Beijing 100021, Peoples R China
6.Peking Univ, Hosp 3, Inst Vasc Med, Beijing 100871, Peoples R China

Recommended Citation:
Wang, Xiaojian,Wang, Jizheng,Su, Ming,et al. TNNI3K, a Cardiac-Specific Kinase, Promotes Physiological Cardiac Hypertrophy in Transgenic Mice[J]. PLOS ONE,2013,8(3).
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