Sarcoplasmic reticulum Ca2+ regulatory protein gene expression in human right atrium under hemodynamic overload
Sarcoplasmic reticulum Ca2+ regulatory protein gene expression in human right atrium under hemodynamic overload
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血流动力学超负荷下人右心房肌浆网Ca2调节蛋白基因表达
DOI：
10.1007/bf01747849
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发表时间：
2005
影响因子：
1.5
通讯作者：
A. Takeshita
中科院分区：
文献类型：
--
作者：
K. Sadamatsu;Y. Urabe;H. Tsutsui;H. Tagawa;F. Maruoka;K. Igarashi;K. Takeda;Y. Kawachi;H. Yasui;A. Takeshita
肌浆网（SR）Ca ~（2+）-腺苷三磷酸酶（ATP酶）mRNA表达在衰竭的人心肌中降低。然而，目前尚不清楚SR Ca 2 +-调节蛋白基因表达是否在人心肌组织中受到压力超负荷或容量超负荷的改变。我们试图确定是否SR Ca 2+调节蛋白基因表达的改变，在人类心房组织进行机械过载。我们在心内直视手术中从三组患者中获得右心房心肌组织（约250 mg）：无右心房血流动力学过载（对照组; 12例患者），房间隔缺损（ASD组; 8例患者）和三尖瓣返流（TR组; 7例患者）。我们测量了心肌细胞大小、间质纤维化面积、SR Ca 2 +-ATP酶和ryanodine受体mRNA丰度。离体心肌细胞面积和间质纤维化面积百分比均为TR > ASD >对照组（P < 0.05）。SR Ca ~（2+）-ATP酶mRNA水平在TR组明显低于对照组（P = 0.004），而在ASD组与对照组无明显差异。三组间Ryanodine受体mRNA水平无显著差异。SR Ca ~（2+）-ATP酶基因表达在TR患者心房组织中下调，而在ASD患者心房组织中未下调，这可能与心肌血流动力学负荷的程度和/或类型不同有关。
SummarySarcoplasmic reticulum (SR) Ca2+-adenosine triphosphatase (ATPase) mRNA expression is reduced in the failing human myocardium. However, it is not known whether SR Ca2+-regulatory protein gene expression is altered in human myocardial tissue subjected to pressure overload or volume overload. We sought to determine whether SR Ca2+-regulatory protein gene expression is altered in human atrial tissue subjected to mechanical overload. We obtained right atrial myocardial tissue (about 250mg) at open-heart surgery from three groups of patients: no hemodynamic overload to the right atrium (control group; 12 patients), atrial septal defect (ASD group; 8 patients), and tricuspid regurgitation (TR group; 7 patients). We measured the myocyte size, the area of interstitial fibrosis, SR Ca2+-ATPase, and ryanodine receptor mRNA abundance. The isolated cardiocyte area and the percent area of interstitial fibrosis were in the order TR > ASD > control (P < 0.05). The SR Ca2+-ATPase mRNA level in TR was significantly decreased (P = 0.004) compared with the control, whereas in the ASD group it did not differ significantly from control. There were no significant differences in ryanodine receptor mRNA levels among the three groups. SR Ca2+-ATPase gene expression was downregulated in human atrial tissue with TR but not in ASD, which might have resulted from the differences in the degree and/or the type of hemodynamic overload to the myocardium.
细胞内钙调节异常是心脏收缩功能障碍的主要原因。
DOI：
10.1056/nejm199108293250906
发表时间：
1991
期刊：
The New England journal of medicine
影响因子：
--
作者：
Morgan,JP
通讯作者：
Morgan,JP