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Article: Temporal relationship of autophagy and apoptosis in neurons challenged by low molecular weight β-amyloid peptide

TitleTemporal relationship of autophagy and apoptosis in neurons challenged by low molecular weight β-amyloid peptide
Authors
Keywordsβ-amyloid
Alzheimer's disease
Apoptosis
Autophagy
Death associated protein kinase
Issue Date2011
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1582-1838
Citation
Journal Of Cellular And Molecular Medicine, 2011, v. 15 n. 2, p. 244-257 How to Cite?
AbstractAlzheimer's disease (AD) is an aging-related progressive neurodegenerative disorder. Previous studies suggested that various soluble Aβ species are neurotoxic and able to activate apoptosis and autophagy, the type I and type II programmed cell death, respectively. However, the sequential and functional relationships between these two cellular events remain elusive. Here we report that low molecular weight Aβ triggered cleavage of caspase 3 and poly (ADP-ribose) polymerase to cause neuronal apoptosis in rat cortical neurons. On the other hand, Aβ activated autophagy by inducing autophagic vesicle formation and autophagy related gene 12 (ATG12), and up-regulated the lysoso-mal machinery for the degradation of autophagosomes. Moreover, we demonstrated that activation of autophagy by Aβ preceded that of apoptosis, with death associated protein kinase phosphorylation as the potential molecular link. More importantly, under Aβ toxicity, neurons exhibiting high level of autophagosome formation were absent of apoptotic features, and inhibition of autophagy by 3-methylade-nine advanced neuronal apoptosis, suggesting that autophagy can protect neurons from Aβ-induced apoptosis. © 2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/133575
ISSN
2012 Impact Factor: 4.753
2015 SCImago Journal Rankings: 1.941
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant Council GRF7552/06M
7616/09M
N_HKU707/07M
HKU200811159082
HKU Alzheimer's Disease Research Network
Graduate School
University of Hong Kong
Funding Information:

This work was supported by Research Grant Council GRF (7552/06M, 7616/09M), N_HKU (707/07M), HKU Seed Funding for Basic Research (200811159082) and HKU Alzheimer's Disease Research Network. YTC, NQZ, CHLH and CSWL are supported by the Graduate School and MSY is supported by Postdoctoral Fellowship from The University of Hong Kong. Confocal live-cell imaging was supported by Faculty Core Facility.

References

 

DC FieldValueLanguage
dc.contributor.authorCheung, YTen_HK
dc.contributor.authorZhang, NQen_HK
dc.contributor.authorHung, CHLen_HK
dc.contributor.authorLai, CSWen_HK
dc.contributor.authorYu, MSen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorChang, RCCen_HK
dc.date.accessioned2011-05-24T02:11:02Z-
dc.date.available2011-05-24T02:11:02Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Cellular And Molecular Medicine, 2011, v. 15 n. 2, p. 244-257en_HK
dc.identifier.issn1582-1838en_HK
dc.identifier.urihttp://hdl.handle.net/10722/133575-
dc.description.abstractAlzheimer's disease (AD) is an aging-related progressive neurodegenerative disorder. Previous studies suggested that various soluble Aβ species are neurotoxic and able to activate apoptosis and autophagy, the type I and type II programmed cell death, respectively. However, the sequential and functional relationships between these two cellular events remain elusive. Here we report that low molecular weight Aβ triggered cleavage of caspase 3 and poly (ADP-ribose) polymerase to cause neuronal apoptosis in rat cortical neurons. On the other hand, Aβ activated autophagy by inducing autophagic vesicle formation and autophagy related gene 12 (ATG12), and up-regulated the lysoso-mal machinery for the degradation of autophagosomes. Moreover, we demonstrated that activation of autophagy by Aβ preceded that of apoptosis, with death associated protein kinase phosphorylation as the potential molecular link. More importantly, under Aβ toxicity, neurons exhibiting high level of autophagosome formation were absent of apoptotic features, and inhibition of autophagy by 3-methylade-nine advanced neuronal apoptosis, suggesting that autophagy can protect neurons from Aβ-induced apoptosis. © 2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.en_HK
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1582-1838en_HK
dc.relation.ispartofJournal of Cellular and Molecular Medicineen_HK
dc.rightsThe definitive version is available at www3.interscience.wiley.com-
dc.subjectβ-amyloiden_HK
dc.subjectAlzheimer's diseaseen_HK
dc.subjectApoptosisen_HK
dc.subjectAutophagyen_HK
dc.subjectDeath associated protein kinaseen_HK
dc.titleTemporal relationship of autophagy and apoptosis in neurons challenged by low molecular weight β-amyloid peptideen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1582-1838&volume=15&issue=2&spage=244&epage=257&date=2011&atitle=Temporal+relationship+of+autophagy+and+apoptosis+in+neurons+challenged+by+low+molecular+weight+β-amyloid+peptide-
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailChang, RCC:rccchang@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityChang, RCC=rp00470en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1582-4934.2009.00990.xen_HK
dc.identifier.pmid20015199-
dc.identifier.scopuseid_2-s2.0-79951907564en_HK
dc.identifier.hkuros185090en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79951907564&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume15en_HK
dc.identifier.issue2en_HK
dc.identifier.spage244en_HK
dc.identifier.epage257en_HK
dc.identifier.eissn1582-4934-
dc.identifier.isiWOS:000287749000007-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridCheung, YT=16678256500en_HK
dc.identifier.scopusauthoridZhang, NQ=44561737000en_HK
dc.identifier.scopusauthoridHung, CHL=44561183300en_HK
dc.identifier.scopusauthoridLai, CSW=26022547000en_HK
dc.identifier.scopusauthoridYu, MS=35346047600en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.scopusauthoridChang, RCC=7403713410en_HK
dc.identifier.citeulike8883710-

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