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期刊论文

Increased expression of calcium-sensing receptors induced by ox-LDL amplifiesapoptosis of cardiomyocytes during simulated ischaemia-reperfusion

徐长庆Jin Guo*§ Hong-Zhu Li* Wei-Hua Zhang*? Lu-Chuan Wang Li-Na Wang* Li Zhang* Guang-Wei Li* Hong-Xia Li* Bao-Feng Yang?? Lingyun Wu*** Rui Wang*** and Chang-Qing Xu*?

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摘要/描述

1. Acute myocardial infarction (AMI) is strongly associatedwith atherosclerosis, and is responsible for significant morbidityand mortality worldwide. The pathogenic mechanisms thatunderlie atherosclerosis and AMI are undefined at present. Thecalcium-sensing receptor (CaSR) is a member of the superfamilyof G-protein coupled receptors. It has been demonstrated previouslythat the expression of CaSR is increased in atheroscleroticcardiac tissue of rats. It has also been suggested that CaSR has acrucial role in cardiac ischaemia–reperfusion injury, apoptosisand hypertrophy. However, it remains to be determined whetheran increase in the expression of CaSR influences the sensitivity ofcardiomyocytes to AMI.2. The present study used cultured ventricular cardiomyocytesfrom neonatal rats to investigate the effect of oxidized low-densitylipoprotein (ox-LDL), ischaemia–reperfusion, GdCl3 (an agonistof CaSR) and NPS-2390 (an antagonist of CaSR) on the expressionof CaSR. The amount of apoptosis, alterations in the morphologyof the cells, the intracellular calcium concentration([Ca2+]i) and components of critical mitochondrial pathwayswere also analysed.3. Cardiomyocytes treated with ox-LDL showed upregulatedexpression of CaSR, cytochrome c (cyt-c), Bax and activated caspase3 (17 kD) and downregulated expression of Bcl-2, as well aselevated [Ca2+]i and apoptosis. Application of GdCl3 augmentedthese effects, and NPS-2390 decreased the expression of CaSRand reduced apoptosis.4. In conclusion, ox-LDL was found to increase the expressionof CaSR in a manner that was dependent on time anddose. It also augmented apoptosis during simulated ischaemia-reperfusion in cultured ventricular cardiomyocytes fromneonatal rats.

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