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首页> 外文期刊>American Journal of Physiology >In vivo administration of calpeptin attenuates calpain activation and cardiomyocyte loss in pressure-overloaded feline myocardium
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In vivo administration of calpeptin attenuates calpain activation and cardiomyocyte loss in pressure-overloaded feline myocardium

机译：钙蛋白酶的体内给药可减轻压力超负荷猫心肌中钙蛋白酶的活化和心肌细胞的损失

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摘要

Calpain activation is linked to the cleavage of several cytoskeletal proteins and could be an important contributor to the loss of cardiomyocytes and contractile dysfunction during cardiac pressure overload (PO). Using a feline right ventricular (RV) PO model, we analyzed calpain activation during the early compensatory period of cardiac hypertrophy. Calpain enrichment and its increased activity with a reduced calpastatin level were observed in 24- to 48-h-PO myocardium, and these changes returned to basal level by 1 wk of PO. Histochemical studies in 24-h-PO myocardium revealed the presence of TdT-mediated dUTP nick-end label (TUNEL)-positive cardiomyocytes, which exhibited enrichment of calpain and gelsolin. Biochemical studies showed an increase in histone H2B phosphorylation and cytoskeleta) binding and cleavage of gelsolin, which indicate programmed cardiomyocyte cell death.
机译：钙蛋白酶的激活与几种细胞骨架蛋白的裂解有关，并且可能是导致心脏压力超负荷（PO）期间心肌细胞丢失和收缩功能障碍的重要因素。使用猫右心室（RV）PO模型，我们分析了心肌肥大的早期代偿期的钙蛋白酶激活。在24-48-h-PO心肌中观察到钙蛋白酶富集及其活性的增加和钙蛋白酶抑素水平的降低，并且这些变化在1 wk PO时恢复到基础水平。在24-h-PO心肌中的组织化学研究表明，存在TdT介导的dUTP缺口末端标记（TUNEL）阳性心肌细胞，表现出钙蛋白酶和凝溶胶蛋白的富集。生化研究表明，组蛋白H2B磷酸化和细胞骨架的结合以及凝溶胶蛋白的裂解均增加，这表明程序性心肌细胞死亡。

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