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Conference Paper: Differential signaling of unfolded protein responses (UPR) and endoplasmic reticulum (ER) stress in neurons exposed to β-amyloid peptide

TitleDifferential signaling of unfolded protein responses (UPR) and endoplasmic reticulum (ER) stress in neurons exposed to β-amyloid peptide
Authors
KeywordsAPOPTOSIS
NEUROTOXICITY
SIGNAL TRANSDUCTION
PROTEIN KINASE
Issue Date2004
PublisherSociety for Neuroscience
Citation
Neuroscience 2004, San Diego, CA, 23-27 October 2004, Presentation no. 1000.22 How to Cite?
AbstractAccumulation of β-amyloid (Aβ) peptide has long been considered as one of the toxic factors contributing to the progression of neurodegeneration in Alzheimer’s disease (AD). It has previously been demonstrated that Aβ peptide triggers release of calcium from the ER. Since calcium plays important roles in the proper folding of protein in the ER, depletion of ER calcium has been considered to be a factor inducing UPR. The aim of this study is to examine the signaling mechanisms of UPR. While Aβ peptide induced calcium release from the ER in primary cultured cortical neurons, it could not stimulate the phosphorylation of PKR-like ER kinase (PERK). In addition, no alternative splicing of Xbp1 mRNA or upregulation of its mRNA were detected suggesting that no activation of ATF6 and Ire1 in neurons exposed to Aβ peptide. Although UPR is not observed, increased protein levels of Grp78, mRNA levels of Gadd153, cleavage of caspase-12 and activity of caspase-7 were detected 16 h after exposure to Aβ peptide. The results suggest that signaling of UPR and ER stress responses can be two separated events. While neuronal apoptosis occurred prior to the signaling of ER stress response, ER stress responses are not the early apoptotic events mediating neuronal apoptosis. Supported by Procore-France/Hong Kong Joint Research Scheme (F-HK21/03T) to RCCC & JH ; HKU Seed Funding for Basic Research (2004) to RCCC
Persistent Identifierhttp://hdl.handle.net/10722/95574

 

DC FieldValueLanguage
dc.contributor.authorChang, RCCen_HK
dc.contributor.authorYu, MSen_HK
dc.contributor.authorSuen, KCen_HK
dc.contributor.authorLai, SWen_HK
dc.contributor.authorKwok, NSen_HK
dc.contributor.authorHugon, Jen_HK
dc.date.accessioned2010-09-25T16:06:32Z-
dc.date.available2010-09-25T16:06:32Z-
dc.date.issued2004en_HK
dc.identifier.citationNeuroscience 2004, San Diego, CA, 23-27 October 2004, Presentation no. 1000.22en_HK
dc.identifier.urihttp://hdl.handle.net/10722/95574-
dc.description.abstractAccumulation of β-amyloid (Aβ) peptide has long been considered as one of the toxic factors contributing to the progression of neurodegeneration in Alzheimer’s disease (AD). It has previously been demonstrated that Aβ peptide triggers release of calcium from the ER. Since calcium plays important roles in the proper folding of protein in the ER, depletion of ER calcium has been considered to be a factor inducing UPR. The aim of this study is to examine the signaling mechanisms of UPR. While Aβ peptide induced calcium release from the ER in primary cultured cortical neurons, it could not stimulate the phosphorylation of PKR-like ER kinase (PERK). In addition, no alternative splicing of Xbp1 mRNA or upregulation of its mRNA were detected suggesting that no activation of ATF6 and Ire1 in neurons exposed to Aβ peptide. Although UPR is not observed, increased protein levels of Grp78, mRNA levels of Gadd153, cleavage of caspase-12 and activity of caspase-7 were detected 16 h after exposure to Aβ peptide. The results suggest that signaling of UPR and ER stress responses can be two separated events. While neuronal apoptosis occurred prior to the signaling of ER stress response, ER stress responses are not the early apoptotic events mediating neuronal apoptosis. Supported by Procore-France/Hong Kong Joint Research Scheme (F-HK21/03T) to RCCC & JH ; HKU Seed Funding for Basic Research (2004) to RCCC-
dc.languageengen_HK
dc.publisherSociety for Neuroscience-
dc.relation.ispartofSociety for Neuroscience Annual Meetingen_HK
dc.subjectAPOPTOSIS-
dc.subjectNEUROTOXICITY-
dc.subjectSIGNAL TRANSDUCTION-
dc.subjectPROTEIN KINASE-
dc.titleDifferential signaling of unfolded protein responses (UPR) and endoplasmic reticulum (ER) stress in neurons exposed to β-amyloid peptideen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailChang, RCC: rccchang@hkucc.hku.hken_HK
dc.identifier.emailYu, MS: ymsmabel@graduate.hku.hken_HK
dc.identifier.emailLai, SW: coralai@ymail.comen_HK
dc.identifier.authorityChang, RCC=rp00470en_HK
dc.identifier.hkuros96478en_HK

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