PI3K-ERK1/2 activation contributes to extracellular H2O2 generation in amyloid beta toxicity

Cited 11 time in scopus
Metadata Downloads

Full metadata record

DC FieldValueLanguage
dc.contributor.authorJong Seong Ha-
dc.contributor.authorHye Yeong Sung-
dc.contributor.authorH M Lim-
dc.contributor.authorKi Sun Kwon-
dc.contributor.authorSung Sup Park-
dc.date.accessioned2017-04-19T09:35:24Z-
dc.date.available2017-04-19T09:35:24Z-
dc.date.issued2012-
dc.identifier.issn0304-3940-
dc.identifier.uri10.1016/j.neulet.2012.08.023ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11023-
dc.description.abstractAmyloid β peptide (Aβ) induces hydrogen peroxide (H2O2) and superoxide generation, leading to neuronal death. Many studies have shown the involvement of NADPH oxidase, but the isotype-specific role was not assessed. Moreover, the activation status of phosphoinositide 3-kinase (PI3K) and extracellular signal-regulated kinase (ERK) 1/2 is unclear in extracellular H2O2 generation. In this paper, we showed that Aβ1-42 induced extracellular H2O2 generation and the resulting cytotoxicity in a concentration-dependent manner. Nox2- and Nox4-specific siRNAs suppressed H2O2 and superoxide generation. LY294002 and U0126, inhibitors of PI3K and ERK1/2, respectively, reduced H2O2 generation in concentration-dependent manners. Furthermore, PI3K activation is responsible for ERK1/2 phosphorylation. An additional increase in H2O2 generation and corresponding cytotoxicity was observed after treatment with Aβ1-42 and glutamate. These results suggest that Aβ1-42 enhances the neuronal vulnerability to oxidative injury in Alzheimer's disease (AD) by increasing H2O2 generation.-
dc.publisherElsevier-
dc.titlePI3K-ERK1/2 activation contributes to extracellular H2O2 generation in amyloid beta toxicity-
dc.title.alternativePI3K-ERK1/2 activation contributes to extracellular H2O2 generation in amyloid beta toxicity-
dc.typeArticle-
dc.citation.titleNeuroscience Letters-
dc.citation.number2-
dc.citation.endPage117-
dc.citation.startPage112-
dc.citation.volume526-
dc.contributor.affiliatedAuthorJong Seong Ha-
dc.contributor.affiliatedAuthorHye Yeong Sung-
dc.contributor.affiliatedAuthorKi Sun Kwon-
dc.contributor.affiliatedAuthorSung Sup Park-
dc.contributor.alternativeName하종성-
dc.contributor.alternativeName성혜영-
dc.contributor.alternativeName임헌-
dc.contributor.alternativeName권기선-
dc.contributor.alternativeName박성섭-
dc.identifier.bibliographicCitationNeuroscience Letters, vol. 526, no. 2, pp. 112-117-
dc.identifier.doi10.1016/j.neulet.2012.08.023-
dc.subject.keywordAmyloid peptide-
dc.subject.keywordOxidative stress-
dc.subject.keywordNADPH oxidase-
dc.subject.keywordPI3K-
dc.subject.keywordERK1/2-
dc.subject.localAmyloid peptide-
dc.subject.localOxidative stre-
dc.subject.localOxidative stress-
dc.subject.localOXIDATIVE STRESS-
dc.subject.localOxidative Stress-
dc.subject.localoxidative stress-
dc.subject.localNADPH oxidase-
dc.subject.localPI3-K-
dc.subject.localPI3K-
dc.subject.localERK1/2-
dc.description.journalClassY-
Appears in Collections:
Aging Convergence Research Center > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.