کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
10738463 1046706 2011 16 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Neuroprotective effects of overexpressed cyclophilin B against Aβ-induced neurotoxicity in PC12 cells
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی سالمندی
پیش نمایش صفحه اول مقاله
Neuroprotective effects of overexpressed cyclophilin B against Aβ-induced neurotoxicity in PC12 cells
چکیده انگلیسی
Accumulated amyloid-β (Aβ) is a well-known cause of neuronal apoptosis in Alzheimer disease and functions in part by generating oxidative stress. Our previous work suggested that cyclophilin B (CypB) protects against endoplasmic reticulum (ER) stress. Therefore, in this study we examined the ability of CypB to protect against Aβ toxicity. CypB is present in the neurons of rat and mouse brains, and treating neural cells with Aβ25-35 mediates apoptotic cell death. Aβ25-35-induced neuronal toxicity was inhibited by the overexpression of CypB as measured by cell viability, apoptotic morphology, sub-G1 cell population, intracellular reactive oxygen species accumulation, activated caspase-3, PARP cleavage, Bcl-2 proteins, mitogen-activated protein kinase (MAPK) activation, and phosphoinositide 3-kinase (PI-3-K) activation. CypB/R95A PPIase mutants did not reduce Aβ25-35 toxicity. We showed that Aβ25-35-induced apoptosis is more severe in a CypB knockdown model, confirming that CypB protects against Aβ25-35-induced toxicity. Consequently, these findings suggest that CypB may protect against Aβ toxicity by its antioxidant properties, by regulating MAPK and PI-3-K signaling, and through the ER stress pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 51, Issue 4, 15 August 2011, Pages 905-920
نویسندگان
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