Molecular mechanisms of Ca^<2+> uptake by sarcolipin in cardiac sarcoplasmic reticulum.

心脏肌浆网肌磷脂摄取Ca ^ 2 的分子机制。

基本信息

  • 批准号:
    16500269
  • 负责人:
  • 金额:
    $ 1.66万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2004
  • 资助国家:
    日本
  • 起止时间:
    2004 至 2006
  • 项目状态:
    已结题

项目摘要

The aim of the study was to explore the role of Ca^<2+> handling-related protein, sarcolipin (SLN) for the regulation of intracellular Ca^<2+> concentration. Sarcoplasmic reticulum (SR)(SERCA2a) is regulated by phospholamban (PLB) and SLN which couple with SERCA2a. Both non-phosphorylated-PLB and -SLN decrease the Ca^<2+> uptake rate of SR. We overexpressed SLN in ventricular muscles of mouse (SLN-TG) and investigated how SERCA2a is influenced by SLN. We measured the Ca^<2+> transients and contraction in intact left ventricular papillary muscles of mouse using the aequorin method. Also, we used saponin-treated thin trabeculae to investigate Ca^<2+> uptake, Ca^<2+> release and Ca^<2+> leakage. In twitch contraction, Hz, the peaks of the Ca^<2+> transient and contraction in SLN-TG were lower than those of the control. The rate of decline of the Ca^<2+> transient and tension was slower than that of the control. In the skinned fiber, Ca^<2+> was loaded in the SR in the presence of ATP and Ca^<2+> (pCa 6.2) for various periods, and Ca^<2+> in the SR was released by caffeine. We measured the released Ca^<2+> with fluo-3. The rate of Ca^<2+> uptake in SLN-TG was slower when the Ca^<2+> loading time was short but no difference was observed when the loading time was longer. The maximal Ca^<2+> content of SR at a steady state in both TG and non-TG cardiac muscles did not differ. Ca^<2+>-induced Ca^<2+> release (CICR) in SLN-TG did not differ from that in non-TG. Ca^<2+> leakage was estimated by measuring the leaked Ca in the solution without ATP and Ca^<2+> after Ca^<2+> loading. Ca^<2+> leakage in SLN-TG was not different from that in non-TG. Thus, SLN decreases the Ca^<2+> uptake in SR and influences intracellular Ca^<2+> concentration. The role of SLN is significant in beat-to-beat contraction, but SLN does not play a significant role at a steady state.
本研究旨在探讨钙处理相关蛋白肌磷脂(sarcolipin,SLN)对细胞内钙离子浓度的调节作用。肌浆网(SR)(SERCA 2a)受受磷蛋白(PLB)和SLN的调节,SLN与SERCA 2a偶联。非磷酸化的-PLB和-SLN均降低SR的Ca^2+摄取速率。我们在小鼠心室肌中过表达SLN(SLN-TG),并研究了SLN如何影响SERCA 2a。我们用水母发光蛋白法测定了小鼠完整左心室乳头肌的Ca^<2+>瞬变和收缩。此外,我们还用皂苷处理的薄骨小梁研究Ca^2+摄取、Ca^2+释放和Ca^2+渗漏。SLN-TG的颤搐收缩频率、Ca^2+瞬变峰和收缩峰均低于对照组。Ca^<2+>瞬变和张力的下降速度比对照组慢。在去皮纤维中,在ATP和Ca^<2+>(pCa 6.2)存在的情况下,SR中的Ca^<2+>被负载不同的时间,并且SR中的Ca^<2+>被咖啡因释放。我们用fluo-3测量了释放的Ca^<2+>。钙负荷时间越短,SLN-TG的钙摄取速率越慢,而钙负荷时间越长,两者之间无明显差异。TG和非TG心肌中稳态SR的最大Ca^<2+>含量没有差异。钙诱导的钙释放(CICR)在SLN-TG和non-TG中没有差异。通过测量不含ATP的溶液中泄漏的Ca和Ca^<2+>负载后的Ca^<2 +>来估计Ca^<2 +>泄漏。SLN-TG组与非TG组的Ca^<2+>渗漏无明显差异。因此,SLN可降低SR对Ca^2+的摄取,从而影响细胞内Ca^2+浓度。SLN在搏动收缩中的作用是显著的,但在稳态下SLN不起显著作用。

项目成果

期刊论文数量(12)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Evaluation of the cross-bridge-dependent change in the Ca2+ affinity of troponin C in aequorin-injected ferret ventricular muscles
  • DOI:
    10.1016/j.ceca.2004.08.003
  • 发表时间:
    2005-02-01
  • 期刊:
  • 影响因子:
    4
  • 作者:
    Ishikawa, T;O-Uchi, J;Kurihara, S
  • 通讯作者:
    Kurihara, S
Comparative effects of bupivacaine and ropivacaine on intracellular calcium transients and tension in ferret ventricular muscle
布比卡因和罗哌卡因对雪貂心室肌细胞内钙瞬变和张力的比较影响
  • DOI:
  • 发表时间:
    2004
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Mio Y
  • 通讯作者:
    Mio Y
Presenilin 2 regulates the systolic function of heart by modulating Ca2+ signaling
  • DOI:
    10.1096/fj.05-3744fje
  • 发表时间:
    2005-12
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Toshihiro Takeda;M. Asahi;O. Yamaguchi;S. Hikoso;H. Nakayama;Y. Kusakari;M. Kawai;K. Hongo;
  • 通讯作者:
    Toshihiro Takeda;M. Asahi;O. Yamaguchi;S. Hikoso;H. Nakayama;Y. Kusakari;M. Kawai;K. Hongo;
p38α mitogen-activated protein kinase plays a critical role in cardiomyocyte survival but not in cardiac hypertrophic growth in response to pressure overload
  • DOI:
    10.1128/mcb.24.24.10611-10620.2004
  • 发表时间:
    2004-12-01
  • 期刊:
  • 影响因子:
    5.3
  • 作者:
    Nishida, K;Yamaguchi, O;Otsu, K
  • 通讯作者:
    Otsu, K
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KURIHARA Satoshi其他文献

KURIHARA Satoshi的其他文献

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{{ truncateString('KURIHARA Satoshi', 18)}}的其他基金

Proposal of adaptive coordination formation control mechanism for multiagent planning
多智能体规划自适应协调编队控制机制的提出
  • 批准号:
    23300058
  • 财政年份:
    2011
  • 资助金额:
    $ 1.66万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Proposal of hierarchy structure emergence mechanism for large scale complex systems
大规模复杂系统层次结构涌现机制的提出
  • 批准号:
    23650071
  • 财政年份:
    2011
  • 资助金额:
    $ 1.66万
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
Molecular mechanisms of an improvement in prognosis in the mouse model of dilated cardiomyopathy treated by inhibition of the RAA system
抑制 RAA 系统治疗扩张型心肌病小鼠模型预后改善的分子机制
  • 批准号:
    22300130
  • 财政年份:
    2010
  • 资助金额:
    $ 1.66万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Proposal of top-down controllable multiagent coordination mechanism
自上而下的可控多主体协调机制的提出
  • 批准号:
    20500133
  • 财政年份:
    2008
  • 资助金额:
    $ 1.66万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Molecular mechanism of contractile dysfunction and the alteration of intracellular Ca^<2+> handling caused by mutation of cardiac troponin T
心肌肌钙蛋白T突变引起收缩功能障碍及细胞内Ca^2处理改变的分子机制
  • 批准号:
    19500357
  • 财政年份:
    2007
  • 资助金额:
    $ 1.66万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Research on assessment system of medical dental students' clinical competence before entering clinical clerkship
医学牙科学生进入临床实习前临床能力评价体系研究
  • 批准号:
    13800002
  • 财政年份:
    2001
  • 资助金额:
    $ 1.66万
  • 项目类别:
    Grant-in-Aid for Special Purposes
A Basis Study of Ethnographies in Southwest of China -Mainly Yunnan Area-
西南地区——主要是云南地区——民族志基础研究
  • 批准号:
    13610368
  • 财政年份:
    2001
  • 资助金额:
    $ 1.66万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Production of new recombinant aequorin and its physiological application
新型重组水母发光蛋白的制备及其生理应用
  • 批准号:
    13557004
  • 财政年份:
    2001
  • 资助金额:
    $ 1.66万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Intracellular Ca^<2+> regulation in the myocardium with ryanodine receptor type 2(+/-) heterozygous mouse
兰尼定受体2型(/-)杂合小鼠心肌细胞内Ca^<2>调节
  • 批准号:
    13670048
  • 财政年份:
    2001
  • 资助金额:
    $ 1.66万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Molecular Mechanisms of Active Cross-bridge-dependent Regulation of Ca affinity of Cardiac Troponin
心肌肌钙蛋白 Ca 亲和力的主动跨桥依赖性调节的分子机制
  • 批准号:
    10470010
  • 财政年份:
    1998
  • 资助金额:
    $ 1.66万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B).

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Critical Sorting Steps and Pathways in the Trafficking of Cardiac Sarcoplasmic Reticulum Proteins
心脏肌浆网蛋白运输的关键分选步骤和途径
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