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首页> 外文期刊>Life sciences >Delayed cytoprotection induced by hypoxic preconditioning in cultured neonatal rat cardiomyocytes: Role of GRP78
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Delayed cytoprotection induced by hypoxic preconditioning in cultured neonatal rat cardiomyocytes: Role of GRP78

机译：低氧预处理在培养的新生大鼠心肌细胞中诱导的延迟细胞保护：GRP78的作用

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摘要

Hypoxic preconditioning (HPC) has been well demonstrated to have potent protective effects in many cell types; however, the mechanisms responsible for this phenomenon are not fully understood. Recently, glucose-regulated protein 78 (GRP78), an inducible molecular chaperon, was indicated to be associated with ischemic preconditioning. We hypothesized that HPC protects cardiomyocytes against hypoxia by inducing GRP78 in cultured neonatal rat cardiomyocytes. HPC was induced by exposing cardiomyocytes to brief hypoxia (1% O-2, 30 min) followed by reoxygenation. GRP78 was expressed constitutively in cultured cardiomyocytes and its expression was enhanced at 12 It, peaked at 24 h (207.3 +/- 23.6% of the baseline), and was sustained for up to 72 h after HPC. Twenty-four hours after HPC, the myocytes were subjected to prolonged hypoxia (1% 0,, 12 h). The lactic dehydrogenase (LDH) release and malondialdehyde (NIDA) content were reduced, while cell viability and superoxide dismutase (SOD) activity were increased in the preconditioned cells compared with the non-HPC cells. The GRP78 protein level was higher in cells exposed to both HPC and hypoxia than in the cells exposed to HPC alone or hypoxia alone. Heat shock protein 70 (HSP70) was induced in parallel by late HPC. Transfection of GRP78 antisense oligonucleotides blocked GRP78 expression but not HSP70, resulting in attenuated cardioprotection afforded by late HPC. Furthermore, inducing GRP78 by gene transfer protected cardiomyocytes from hypoxic injury. These findings demonstrate that the induction of GRP78 partially mediates the late HPC, suggesting that GRP78 is a novel mechanism responsible for the late cytoprotection of HPC. (C) 2007 Elsevier Inc. All rights reserved.
机译：缺氧预处理（HPC）已被证明对许多细胞类型具有有效的保护作用。但是，导致这种现象的机制尚未完全了解。最近，表明葡萄糖调节蛋白78（GRP78），一种可诱导的分子伴侣，与缺血预处理相关。我们假设HPC通过在培养的新生大鼠心肌细胞中诱导GRP78来保护心肌细胞免于缺氧。通过将心肌细胞暴露于短暂的缺氧（1％O-2，30分钟），然后再充氧来诱导HPC。 GRP78在培养的心肌细胞中组成性表达，其表达在12 It时增强，在24 h达到峰值（基线的207.3 +/- 23.6％），并在HPC后持续长达72 h。 HPC后二十四小时，对心肌细胞进行长时间缺氧（1％0、12 h）。与非HPC细胞相比，预处理细胞中的乳酸脱氢酶（LDH）释放和丙二醛（NIDA）含量降低，而细胞活力和超氧化物歧化酶（SOD）活性增加。暴露于HPC和缺氧的细胞中的GRP78蛋白水平高于单独暴露于HPC或单独缺氧的细胞。晚期HPC平行诱导热激蛋白70（HSP70）。 GRP78反义寡核苷酸的转染阻断了GRP78的表达，但没有阻断HSP70，导致晚期HPC提供的减弱的心脏保护作用。此外，通过基因转移诱导GRP78可保护心肌细胞免受缺氧损伤。这些发现表明，GRP78的诱导部分地介导了晚期HPC，表明GRP78是负责HPC的晚期细胞保护的新机制。 （C）2007 Elsevier Inc.保留所有权利。

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