부산대학교 도서관

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.neulet.2008.09.020 Byline: Guoying Wu (a), Kenta Nakajima (a), Natsumi Takeyama (c), Masayoshi Yukawa (d), Yojiro Taniuchi (a), Akikazu Sakudo (a)(e), Takashi Onodera (a)(b) Keywords: Prion protein; Species specificity; Apoptosis; Neuroprotection Abstract: The neuroprotective function of prion protein (PrP) was revealed first by the fact that reintroduction of the mouse prion protein gene (Prnp) into a mouse Prnp.sup.-/- neuronal cell line, HpL3-4, could prevent apoptosis induced by serum deprivation. In the present study, the anti-apoptotic activities of mouse, hamster, and bovine PrP were compared by expressing mouse PrP (MoPrP), hamster PrP (HaPrP), and bovine PrP (BoPrP) in HpL3-4 cells, respectively. Morphological analysis and DNA fragmentation assays demonstrated that HpL3-4 cells expressing HaPrP, BoPrP, and empty vector (EM) showed the typical features of apoptosis with DNA laddering and apoptotic bodies after serum deprivation, whereas HpL3-4 cells expressing MoPrP showed decreased levels of apoptosis in comparison. The levels of histone-associated DNA fragments (mono- and oligonucleosomes) in the cytosol fractions of the cells correlated with the levels of DNA laddering. These results indicate a species-specific anti-apoptotic function of PrP exists, suggesting that the interaction of the mouse PrP with mouse host factors is required for its anti-apoptotic activity. Author Affiliation: (a) Department of Molecular Immunology, School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan (b) Research Center for Food Safety, School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan (c) Nippon Institute for Biological Science, Ome 198-0024, Tokyo, Japan (d) Laboratory of Biomedical Science, Department of Veterinary Medicine, College of Biosource Sciences, Nihon University, Fujisawa, Kanagawa 252-8510, Japan (e) Department of Virology, Center for Infectious Disease Control, Research Institute for Microbial Diseases, Osaka University, Yamadaoka, Suita, Osaka 565-0871, Japan Article History: Received 11 August 2008; Revised 9 September 2008; Accepted 9 September 2008