Hypoxia protects neuronal cells from human prion protein fragment-induced apoptosis

Journal of Neurochemistry
Jae-Suk SeoSang-Youel Park

Abstract

Prion diseases are neurodegenerative disorders characterized by the accumulation of an abnormal isoform of the prion protein PrP(Sc). Human prion protein fragment, PrP (106-126) (prion protein peptide 106-126), may contain most of the pathological features associated with PrP(Sc). Hypoxic conditions elicit cellular responses adaptively designed to improve cell survival and have an important role in the process of cell survival. We investigate the effects of hypoxia on PrP (106-126)-induced apoptosis in the present study. Human neuroblastoma and glioblastoma cells were incubated with varied doses of PrP (106-126) under both normoxic or hypoxic conditions, in order to determine the regulatory effects of hypoxia on PrP (106-126)-induced apoptosis. The results indicate that hypoxia protects neuronal cells against PrP (106-126)-induced cell death by activating the Akt signal, which is inactivated by prion proteins, and inhibiting PrP (106-126)-induced caspase 3 activation. Low oxygen conditions increase the Bcl-2 protein, which is associated with anti-apoptotic signals, and recover the PrP (106-126)-induced reduction in mitochondrial transmembrane potential. This study demonstrates that hypoxia inhibits PrP (106-126)-induced neuron ...Continue Reading

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Citations

Jul 8, 2014·International Journal of Molecular Sciences·You-Jin LeeSang-Youel Park
Sep 30, 2010·Biochemical and Biophysical Research Communications·Jae-Kyo JeongSang-Youel Park
Mar 16, 2016·Neurochemical Research·Marcio Henrique Mello da LuzKil Sun Lee
Mar 13, 2013·Cellular & Molecular Biology Letters·Alessandro Didonna
Oct 22, 2013·International Journal of Molecular Medicine·Myung-Hee MoonSang-Youel Park
Aug 1, 2013·International Journal of Molecular Medicine·Jae-Kyo Jeong, Sang-Youel Park
Sep 19, 2014·International Journal of Molecular Medicine·Yang-Gyu Park, Sang-Youel Park

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