首页> 外文期刊>American Journal of Physiology >Antisense inhibition of Na+/Ca2+ exchange during anoxia/reoxygenation in ventricular myocytes.
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Antisense inhibition of Na+/Ca2+ exchange during anoxia/reoxygenation in ventricular myocytes.

机译:心室肌细胞缺氧/复氧过程中Na + / Ca2 +交换的反义抑制。

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摘要

This study investigated the role of the Na+/Ca2+ exchanger (NCX) in regulating cytosolic intracellular Ca2+ concentration ([Ca2+]i) during anoxia/reoxygenation in guinea pig ventricular myocytes. The hypothesis that the NCX is the predominant mechanism mediating [Ca2+]i overload in this model was tested through inhibition of NCX expression by an antisense oligonucleotide. Immunocytochemistry revealed that this antisense oligonucleotide, directed at the area around the start site of the guinea pig NCX1, specifically reduced NCX expression in cultured adult myocytes by 90 +/- 4%. Antisense treatment inhibited evoked NCX activity by 94 +/- 3% and decreased the rise in [Ca2+]i during anoxia/reoxygenation by 95 +/- 3%. These data suggest that NCX is the predominant mechanism mediating Ca2+ overload during anoxia/reoxygenation in guinea-pig ventricular myocytes.
机译:这项研究调查了Na + / Ca2 +交换子(NCX)在调节豚鼠心室肌​​细胞缺氧/复氧过程中胞质内Ca2 +浓度([Ca2 +] i)中的作用。通过反义寡核苷酸抑制NCX表达,检验了NCX是介导[Ca2 +] i超负荷的主要机制这一假设。免疫细胞化学显示,该反义寡核苷酸直接针对豚鼠NCX1起始位点附近的区域,可将成年成年心肌细胞中NCX的表达特异性降低90 +/- 4%。反义处理将诱发的NCX活性抑制了94 +/- 3%,并将缺氧/复氧过程中[Ca2 +] i的升高降低了95 +/- 3%。这些数据表明,NCX是介导豚鼠心室肌​​细胞缺氧/复氧过程中Ca2 +超负荷的主要机制。

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