Gorman Adrienne M, Szegezdi Eva, Quigney Declan J, Samali Afshin
Department of Biochemistry and the National Centre for Biomedical Engineering Science, National University of Ireland, Galway, Ireland.
Biochem Biophys Res Commun. 2005 Feb 18;327(3):801-10. doi: 10.1016/j.bbrc.2004.12.066.
Cellular stress may stimulate cell survival pathways or cell death depending on its severity. 6-Hydroxydopamine (6-OHDA) is a neurotoxin that targets dopaminergic neurons that is often used to induce neuronal cell death in models of Parkinson's disease. Here we present evidence that 6-OHDA induces apoptosis in rat PC12 cells that involves release of cytochrome c and Smac/Diablo from mitochondria, caspase-3 activation, cleavage of PARP, and nuclear condensation. 6-OHDA also induced the heat shock response, leading to increased levels of Hsp25 and Hsp70. Increased Hsp25 expression was associated with cell survival. Prior heat shock or overexpression of Hsp27 (human homologue of Hsp25) delayed cytochrome c release, caspase activation, and reduced the level of apoptosis caused by 6-OHDA. We conclude that 6-OHDA induces a variety of responses in cultured PC12 cells ranging from cell survival to apoptosis, and that induction of stress proteins such as Hsp25 may protect cells from undergoing 6-OHDA-induced apoptosis.
细胞应激根据其严重程度可刺激细胞存活途径或导致细胞死亡。6-羟基多巴胺(6-OHDA)是一种靶向多巴胺能神经元的神经毒素,常用于在帕金森病模型中诱导神经元细胞死亡。在此我们提供证据表明,6-OHDA可诱导大鼠嗜铬细胞瘤(PC12)细胞凋亡,这涉及线粒体细胞色素c和Smac/Diablo的释放、半胱天冬酶-3激活、聚(ADP-核糖)聚合酶(PARP)裂解以及核浓缩。6-OHDA还可诱导热休克反应,导致热休克蛋白25(Hsp25)和热休克蛋白70(Hsp70)水平升高。Hsp25表达增加与细胞存活相关。预先热休克或热休克蛋白27(Hsp25的人类同源物)过表达可延迟细胞色素c释放、半胱天冬酶激活,并降低6-OHDA所致的凋亡水平。我们得出结论,6-OHDA可在培养的PC12细胞中诱导从细胞存活到凋亡的多种反应,并且诱导诸如Hsp25等应激蛋白可能保护细胞免受6-OHDA诱导的凋亡。