The protection of Bcl-2 overexpression on rat cortical neuronal injury caused by analogous ischemia/reperfusion in vitro

Neuroscience Research
Hong ZhangYunliang Guo

Abstract

Recent studies have suggested that neuronal apoptosis in cerebral ischemia could arise from dysfunction of endoplasmic reticulum (ER) and mitochondria. B-cell lymphoma/leukemia-2 gene (Bcl-2) has been described as an inhibitor both in programmed cell death (PCD) and ER dysfunction during apoptosis, and the Bcl-2 family play a key role in regulating the PCD, both locally at the ER and from a distance at the mitochondrial membrane. However, its signal pathways and concrete mechanisms in endoplasmic reticulum-initiated apoptosis remain incompletely understood. We therefore investigate whether ischemia/reperfusion (I/R) causes neuronal apoptosis in part via cross-talk between ER and mitochondria or not, and how the overexpression of Bcl-2 prevents this form of cell death. Here we show that analogous I/R-induced cell death occurs consequent to interactions of ER stress and mitochondrial death pathways. The participation of the mitochondrial pathway was demonstrated by the release of cytochrome C (cyt C) from mitochondrial into cytoplasmic fractions and caspase-9 cleavage. The involvement of ER stress was further supported by the observable increase of glucose-regulated protein 78(GRP78)/BiP expression and caspase-12 activity. Furthe...Continue Reading

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Citations

Mar 5, 2013·Neurological Sciences : Official Journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology·Guoyu ZhouShengnian Zhou
Dec 29, 2015·Acta Pharmacologica Sinica·Yu-shuang ZhangJing Li
Mar 30, 2010·Neuroscience Letters·Shu-Rong DuanDe-Sheng Wang
Sep 18, 2014·Biochemical and Biophysical Research Communications·Jing ZhaoJianlin Wu
Jun 28, 2011·Neurobiology of Aging·Rui O CostaCláudia M F Pereira
Jan 23, 2017·Journal of Neuroinflammation·Wei-Xing ZhaoWei-Dong Mi
Oct 12, 2010·Critical Reviews in Biochemistry and Molecular Biology·Sara BaratchiJagat R Kanwar

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