Autophagic flux induced by graphene oxide has a neuroprotective effect against human prion protein fragments
Jae-Kyo Jeong,1 You-Jin Lee,1 Seung Yol Jeong,2,3 Sooyeon Jeong,2 Geon-Woong Lee,2 Sang-Youel Park1 1Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, 2Nano Hybrid Technology Research Center, Korea Electrotechnology Research Institute (KERI), Changwon...
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| Autores principales: | , , , , , |
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| Formato: | article |
| Lenguaje: | EN |
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Dove Medical Press
2017
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| Acceso en línea: | https://doaj.org/article/5b63750f4c3647a38d7096102ac5502f |
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| Sumario: | Jae-Kyo Jeong,1 You-Jin Lee,1 Seung Yol Jeong,2,3 Sooyeon Jeong,2 Geon-Woong Lee,2 Sang-Youel Park1 1Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, 2Nano Hybrid Technology Research Center, Korea Electrotechnology Research Institute (KERI), Changwon, 3Department of Electrical Functionality Material Engineering, University of Science and Technology (UST), Daejon, Republic of Korea Abstract: Graphene oxide (GO) is a nanomaterial with newly developing biological applications. Autophagy is an intracellular degradation system that has been associated with the progression of neurodegenerative disorders. Although induction of autophagic flux by GO has been reported, the underlying signaling pathway in neurodegenerative disorders and how this is involved in neuroprotection remain obscure. We show that GO itself activates autophagic flux in neuronal cells and confers a neuroprotective effect against prion protein (PrP) (106–126)-mediated neurotoxicity. GO can be detected in SK-N-SH neuronal cells, where it triggers autophagic flux signaling. GO-induced autophagic flux prevented PrP (106–126)-induced neurotoxicity in SK-N-SH cells. Moreover, inactivation of autophagic flux blocked GO-induced neuroprotection against prion-mediated mitochondrial neurotoxicity. This is the first study to demonstrate that GO regulates autophagic flux in neuronal cells, and that activation of autophagic flux signals, induced by GO, plays a neuroprotective role against prion-mediated mitochondrial neurotoxicity. These results suggest that the nanomaterial GO may be used to activate autophagic flux and could be used in neuroprotective strategies for treatment of neurodegenerative disorders, including prion diseases. Keywords: graphene oxide, neuroprotection, autophagy, prion protein, mitochondria |
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