在皮质神经元缺血模型中 caspase 对细胞色素 c 和 AIF 释放的影响的证据。
Evidence for caspase effects on release of cytochrome c and AIF in a model of ischemia in cortical neurons.
机构信息
Department of Biological Sciences, and Neurology and Neurological Sciences, Stanford University, 371 Serra Street, Stanford, CA 94305, USA.
出版信息
Neurosci Lett. 2010 Jan 22;469(2):179-83. doi: 10.1016/j.neulet.2009.11.067. Epub 2009 Nov 26.
Abstract
Neuronal apoptosis following ischemia can be mediated by a caspase-dependent pathway, which involves the mitochondrial release of cytochrome c that initiates a cascade of caspase activation. In addition, there is a caspase-independent pathway, which is mediated by the release of apoptosis-inducing factor (AIF). Using caspase inhibitor gene therapy, we investigated the roles of caspases on the mitochondrial release of cyt c and the release of AIF. Specifically, we used herpes simplex virus-1 amplicon vectors to ectopically express a viral caspase inhibitor (crmA or p35) in mixed cortical cultures exposed to oxygen/glucose deprivation. Overexpression of either crmA or p35 (but not the caspase-3 inhibitor DEVD) inhibited the release of AIF; this suggests that there can be cross-talk between the caspase-dependent and the ostensibly caspase-independent pathway. In addition, both crmA overexpression and DEVD inhibited cyt c release, suggesting a positive feedback loop involving activated caspases stimulating cyt c release.
摘要
缺血后的神经元凋亡可以通过半胱天冬酶依赖性途径介导，该途径涉及细胞色素 c 的线粒体释放，从而引发半胱天冬酶激活级联反应。此外，还有一种不依赖半胱天冬酶的途径，由凋亡诱导因子（AIF）的释放介导。我们使用半胱天冬酶抑制剂基因治疗来研究半胱天冬酶在细胞色素 c 线粒体释放和 AIF 释放中的作用。具体来说，我们使用单纯疱疹病毒 1 扩增子载体在暴露于氧/葡萄糖剥夺的混合皮质培养物中外源性表达病毒半胱天冬酶抑制剂（crmA 或 p35）。crmA 或 p35 的过表达（但不是 caspase-3 抑制剂 DEVD）抑制了 AIF 的释放;这表明 caspase 依赖性途径和表面上不依赖 caspase 的途径之间可能存在串扰。此外，crmA 过表达和 DEVD 均抑制细胞色素 c 的释放，这表明涉及激活的半胱天冬酶刺激细胞色素 c 释放的正反馈回路。
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