Beta-Amyloid Oligomers Activate Apoptotic BAK Pore for Cytochrome c Release
摘要：
In Alzheimer's disease, cytochromec-dependent apoptosis is a crucial pathway in neuronal cell death. Although beta-amyloid (Aβ) oligomers are known to be the neurotoxins responsible for neuronal cell death, the underlying mechanisms remain largely elusive. Here, we report that the oligomeric form of synthetic Aβof 42 amino acids elicits death of HT-22 cells. But, when expression of a bcl-2 family protein BAK is suppressed by siRNA, Aβoligomer-induced cell death was reduced. Furthermore, significant reduction of cytochromecrelease was observed with mitochondria isolated from BAK siRNA-treated HT-22 cells. Our invitro experiments demonstrate that Aβoligomers bind to BAK on the membrane and induce apoptotic BAK pores and cytochromecrelease. Thus, the results suggest that Aβoligomers function as apoptotic ligands and hijack the intrinsic apoptotic pathway to cause unintended neuronal cell death.
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DOI：
10.1016/j.bpj.2014.07.074
被引量：
年份：
2014
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