Molecular basis of junctophilin-2 regulation of ryanodine receptor-2 in cardiomyocytes
心肌细胞中junctophilin-2调节兰尼碱受体2的分子基础
基本信息
- 批准号:RGPIN-2017-04768
- 负责人:
- 金额:$ 2.48万
- 依托单位:
- 依托单位国家:加拿大
- 项目类别:Discovery Grants Program - Individual
- 财政年份:2019
- 资助国家:加拿大
- 起止时间:2019-01-01 至 2020-12-31
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Calcium ion cycling determines heart function and heart muscle cell survival/death. The calcium cycling is regulated by calcium release unit of sarcoplasmic reticulum. This unit keeps calcium cycling properly, a process important for heart contract and relaxation. However, the nature of calcium release unit homeostasis has not been fully understood in heart muscle cells.****This study is proposed to investigate how a structural protein called "junctophilin-2" maintains the normality of calcium release unit in heart muscle cells. Specifically, we will examine how junctophilin-2 protects another protein called “junctin” in heart muscle cells. Junctin is an important component of calcium release unit. Without junctin, calcium release unit does not work properly and increases calcium ion release from sarcoplasmic reticulum, leading to perturbation of calcium homeostasis in cardiomyocytes. Dysregulation of calcium cycling damages heart function. Thus, we will also examine whether protection of junctin is a mechanisms by which junctophilin-2 keeps calcium release unit working properly.****This study will provide molecular basis for junctophilin-2 regulation of junctin in calcium release unit and its influence on calcium cycling. Thus, our findings will significantly increase our understanding of the nature of calcium cycling, which is critical for elucidating mechanistic insights in the biological and pathophysiological states of the heart.***
钙离子循环决定心脏功能和心肌细胞存活/死亡。钙循环受肌浆网钙释放单位的调节。这个单位保持钙循环正常,这是心脏收缩和放松的重要过程。然而,在心肌细胞中,钙释放单位稳态的性质尚未完全了解。本研究拟探讨一种名为“junctophilin-2”的结构蛋白如何维持心肌细胞钙释放单位的正常性。具体来说,我们将研究如何junctophilin-2保护另一种蛋白质称为“连接”在心肌细胞。连接蛋白是钙释放单位的重要组成部分。没有连接蛋白,钙释放单位不能正常工作,增加肌浆网钙离子释放,导致心肌细胞钙稳态紊乱。钙循环失调损害心脏功能。因此,我们还将研究连接蛋白的保护是否是一种机制,通过这种机制,连接蛋白-2保持钙释放单位正常工作。本研究将为研究junctophilin-2对钙释放单位中连接蛋白的调节及其对钙循环的影响提供分子基础。因此,我们的研究结果将显着增加我们对钙循环性质的理解,这对于阐明心脏生物学和病理生理学状态的机制见解至关重要。
项目成果
期刊论文数量(0)
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会议论文数量(0)
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Peng, Tianqing其他文献
Calpain-1 induces endoplasmic reticulum stress in promoting cardiomyocyte apoptosis following hypoxia/reoxygenation.
Calpain-1 诱导内质网应激,促进缺氧/复氧后心肌细胞凋亡。
- DOI:
10.1016/j.bbadis.2015.01.019 - 发表时间:
2015-05 - 期刊:
- 影响因子:6.2
- 作者:
Zheng, Dong;Wang, Grace;Li, Shuai;Fan, Guo-Chang;Peng, Tianqing - 通讯作者:
Peng, Tianqing
Disruption of Rac1 signaling reduces ischemia-reperfusion injury in the diabetic heart by inhibiting calpain
- DOI:
10.1016/j.freeradbiomed.2010.09.018 - 发表时间:
2010-12-01 - 期刊:
- 影响因子:7.4
- 作者:
Shan, Limei;Li, Jianmin;Peng, Tianqing - 通讯作者:
Peng, Tianqing
Rac1 mediates sex difference in cardiac tumor necrosis factor-α expression via NADPH oxidase-ERK1/2/p38 MAPK pathway in endotoxemia
- DOI:
10.1016/j.yjmcc.2009.05.002 - 发表时间:
2009-08-01 - 期刊:
- 影响因子:5
- 作者:
Zhu, Huaqing;Shan, Limei;Peng, Tianqing - 通讯作者:
Peng, Tianqing
Administration of losartan preserves cardiomyocyte size and prevents myocardial dysfunction in tail-suspended mice by inhibiting p47phox phosphorylation, NADPH oxidase activation and MuRF1 expression
- DOI:
10.1186/s12967-019-2021-1 - 发表时间:
2019-08-22 - 期刊:
- 影响因子:7.4
- 作者:
Hang, Liwen;Yuan, Wenyi;Peng, Tianqing - 通讯作者:
Peng, Tianqing
Calpain activation contributes to hyperglycaemia-induced apoptosis in cardiomyocytes
- DOI:
10.1093/cvr/cvp189 - 发表时间:
2009-10-01 - 期刊:
- 影响因子:10.8
- 作者:
Li, Ying;Li, Yanwen;Peng, Tianqing - 通讯作者:
Peng, Tianqing
Peng, Tianqing的其他文献
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{{ truncateString('Peng, Tianqing', 18)}}的其他基金
Molecular basis of junctophilin-2 regulation of ryanodine receptor-2 in cardiomyocytes
心肌细胞中junctophilin-2调节兰尼碱受体2的分子基础
- 批准号:
RGPIN-2017-04768 - 财政年份:2021
- 资助金额:
$ 2.48万 - 项目类别:
Discovery Grants Program - Individual
Molecular basis of junctophilin-2 regulation of ryanodine receptor-2 in cardiomyocytes
心肌细胞中junctophilin-2调节兰尼碱受体2的分子基础
- 批准号:
RGPIN-2017-04768 - 财政年份:2020
- 资助金额:
$ 2.48万 - 项目类别:
Discovery Grants Program - Individual
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