Sarcoplasmic reticulum function in murine ventricular myocytes overexpressing SR CaATPase.
Sarcoplasmic reticulum function in murine ventricular myocytes overexpressing SR CaATPase.
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过度表达 SR CaATPase 的小鼠心室肌细胞的肌浆网功能。
DOI：
10.1006/jmcc.1998.0834
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Barry,WH
中科院分区：
文献类型：
--
作者：
Yao,A;Su,Z;Dillmann,WH;Barry,WH
为了研究肌浆网（SR）CaATP酶过表达对SR和Ca ~（2+）稳态功能的影响，我们用电压钳技术测定了野生型（WT）和转基因（SRTG）小鼠心室肌细胞[Ca ~（2+）] i（fluo-3）、L型Ca ~（2+）电流（伊卡，L）、Na/Ca交换电流（INa/Ca）和SR Ca ~（2+）含量。SRTG心肌细胞[Ca ~（2+）] i幅值增加不明显，而舒张期[Ca ~（2+）] i幅值降低。在SRTG心肌细胞中，[Ca ~（2+）] i的初始和终末下降显著加速，这意味着SR CaATP酶的功能上调。我们研究了只有SR CaATP酶的功能贡献的初始和终末阶段的下降[Ca 2 +]i，突然抑制Na/Ca交换与快速开关设备。与WT心肌细胞相比，SRTG中SR CaATP酶介导的[Ca 2 +]下降率增加了40%。SRTG心肌细胞L-型Ca ~（2+）通道功能无明显变化，但INa/Ca比值略有下降（10%）。测量SR Ca 2+含量显着增加了29%，在SRTG心肌细胞。因此，SR CaATPase的过表达显著加速了[Ca ~（2+）] i的下降，并诱导SR Ca ~（2+）含量的增加，同时伴有Na/Ca交换器的某些下调。
To examine the effects of the overexpression of sarcoplasmic reticulum (SR) CaATPase on function of the SR and Ca2+homeostasis, we measured [Ca2+]itransients (fluo-3), and L-type Ca2+currents (ICa,L), Na/Ca exchanger currents (INa/Ca), and SR Ca2+content with voltage clamp in ventricular myocytes isolated from wild type (WT) mice and transgenic (SRTG) mice. The amplitude of [Ca2+]itransients was insignificantly increased in SRTG myocytes, while the diastolic [Ca2+]itended to be lower. The initial and terminal declines of [Ca2+]itransients were significantly accelerated in SRTG myocytes, implying a functional upregulation of the SR CaATPase. We examined the functional contribution of only the SR CaATPase to the initial and the terminal phase of the decline of [Ca2+]i, by abruptly inhibiting Na/Ca exchange with a rapid switcher device. The rate of [Ca2+] decline mediated by the SR CaATPase was increased by 40% in SRTG compared with WT myocytes. The function of the L-type Ca2+channel was unchanged in SRTG myocytes, while INa/Ca density was slightly (10%) decreased. Measured SR Ca2+content was significantly increased by 29% in SRTG myocytes. Thus, overexpression of SR CaATPase markedly accelerates the decline of [Ca2+]itransients, and induces an increase in SR Ca2+content, with some downregulation of the Na/Ca exchanger.