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: Jeong JK, Lee YJ, Jeong SY, Jeong S, Lee GW, Park SY
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Publicado: Dove Medical Press 2017
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spelling oai:doaj.org-article:5b63750f4c3647a38d7096102ac5502f2021-12-02T05:04:24ZAutophagic flux induced by graphene oxide has a neuroprotective effect against human prion protein fragments1178-2013https://doaj.org/article/5b63750f4c3647a38d7096102ac5502f2017-11-01T00:00:00Zhttps://www.dovepress.com/autophagic-flux-induced-by-graphene-oxide-has-a-neuroprotective-effect-peer-reviewed-article-IJNhttps://doaj.org/toc/1178-2013Jae-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, mitochondriaJeong JKLee YJJeong SYJeong SLee GWPark SYDove Medical PressarticleGraphene oxideneuroprotectionautophagyprion proteinmitochondriaMedicine (General)R5-920ENInternational Journal of Nanomedicine, Vol Volume 12, Pp 8143-8158 (2017)
institution DOAJ
collection DOAJ
language EN
topic Graphene oxide
neuroprotection
autophagy
prion protein
mitochondria
Medicine (General)
R5-920
spellingShingle Graphene oxide
neuroprotection
autophagy
prion protein
mitochondria
Medicine (General)
R5-920
Jeong JK
Lee YJ
Jeong SY
Jeong S
Lee GW
Park SY
Autophagic flux induced by graphene oxide has a neuroprotective effect against human prion protein fragments
description 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
format article
author Jeong JK
Lee YJ
Jeong SY
Jeong S
Lee GW
Park SY
author_facet Jeong JK
Lee YJ
Jeong SY
Jeong S
Lee GW
Park SY
author_sort Jeong JK
title Autophagic flux induced by graphene oxide has a neuroprotective effect against human prion protein fragments
title_short Autophagic flux induced by graphene oxide has a neuroprotective effect against human prion protein fragments
title_full Autophagic flux induced by graphene oxide has a neuroprotective effect against human prion protein fragments
title_fullStr Autophagic flux induced by graphene oxide has a neuroprotective effect against human prion protein fragments
title_full_unstemmed Autophagic flux induced by graphene oxide has a neuroprotective effect against human prion protein fragments
title_sort autophagic flux induced by graphene oxide has a neuroprotective effect against human prion protein fragments
publisher Dove Medical Press
publishDate 2017
url https://doaj.org/article/5b63750f4c3647a38d7096102ac5502f
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AT leeyj autophagicfluxinducedbygrapheneoxidehasaneuroprotectiveeffectagainsthumanprionproteinfragments
AT jeongsy autophagicfluxinducedbygrapheneoxidehasaneuroprotectiveeffectagainsthumanprionproteinfragments
AT jeongs autophagicfluxinducedbygrapheneoxidehasaneuroprotectiveeffectagainsthumanprionproteinfragments
AT leegw autophagicfluxinducedbygrapheneoxidehasaneuroprotectiveeffectagainsthumanprionproteinfragments
AT parksy autophagicfluxinducedbygrapheneoxidehasaneuroprotectiveeffectagainsthumanprionproteinfragments
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