The association between prion proteins and A beta(1-42) oligomers in cytotoxicity and apoptosis
- Authors
- Hyeon, Jae Wook; Kim, Su Yeon; Park, Jun Sun; Choi, Bo Yeong; Lee, Sol Moe; Ju, Young Ran; An, Seong Soo A.; Kim, Chi-Kyeong
- Issue Date
- 27-Jul-2012
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Prion; A beta(1-42) oligomer; Apoptosis; Cell death
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.424, no.2, pp.214 - 220
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 424
- Number
- 2
- Start Page
- 214
- End Page
- 220
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/16276
- DOI
- 10.1016/j.bbrc.2012.06.056
- ISSN
- 0006-291X
- Abstract
- Misfolding of prion protein (PrP to PrPSc) can cause neurodegenerative prion diseases. As a glycosylphosphatidylinositol (GPI)-anchored membrane protein, the normal form of PrP (PrPC) can function as a receptor for ligands in the extracellular space. PrPC was suggested to be involved in memory, synaptic neuronal communication, and anti-oxidation as a neuroprotective agent. The recently identified interaction between PrPC and A beta(1-42) oligomers suggested another role for PrP as a receptor for A beta(1-42) oligomers, thereby influencing cytotoxicity and apoptosis. Here, the association between PrPC and A beta(1-42) oligomers was investigated by visualizing protein localization in neuronal cells by immunocytochemistry. A beta(1-42) oligomer-induced cytotoxicity was tested in respective expressions of PrPC by using mouse neuroblastoma-2a (N2a) cells, the prion protein over-expressed cells (L2-2B1), and a Prnp-null mouse hippocampal cell line (HpL 3-4). Moreover, apoptotic proteins such as caspase-8 were used to assess the effect of PrPC on A beta(1-42) oligomer-mediated apoptosis. In L2-2B1 and HpL 3-4 cells, the difference in the cytotoxicity of A beta(1-42) oligomers could be clearly distinguished. In addition, A beta(1-42) oligomers induced mitochondria dysfunction, reactive oxygen species (ROS) generation, and calcium influx PrPC-dependently. Apoptosis, related to mitochondria dysfunction, was further investigated to determine the cytotoxic pathway; the results suggest that PrPC could be involved in both the intrinsic and extrinsic apoptotic pathways. Finally, cells with abundant PrPC expression seemed to be more susceptible to A beta(1-42) oligomer toxicity, suggesting the importance of the level of PrPC expression in the induction of apoptosis. (C) 2012 Elsevier Inc. All rights reserved.
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