Beta-Amyloid Oligomers Activate Apoptotic BAK Pore for Cytochrome c Release
- Beta-Amyloid Oligomers Activate Apoptotic BAK Pore for Cytochrome c Release
- 김재욱; 양유수; 송승수; 나정현; 오경준; 정철현; 유연규; 신년균
- apoptosis; BAK; beta-amyloid; cytochrome c release
- Issue Date
- Biophysical journal
- VOL 107, NO 7, 1601-1608
- In Alzheimer’s disease, cytochrome c-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 Aβ of 42 amino acids elicits death of HT-22 cells. But, when expression of a bcl-2 family protein BAK is suppressed by siRNA, Aβ oligomer-induced cell death was reduced. Furthermore, significant reduction of cytochrome c release was observed with mitochondria isolated from BAK siRNA-treated HT-22 cells. Our in vitro experiments demonstrate that Aβ oligomers bind to BAK on the membrane and induce apoptotic BAK pores and cytochrome c release. Thus, the results suggest that Aβ oligomers function as apoptotic ligands and hijack the intrinsic apoptotic pathway to cause unintended neuronal cell death.
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