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Article: Effects of all-trans-retinoic acid on human SH-SY5Y neuroblastoma as in vitro model in neurotoxicity research

TitleEffects of all-trans-retinoic acid on human SH-SY5Y neuroblastoma as in vitro model in neurotoxicity research
Authors
Issue Date2009
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuro
Citation
Neurotoxicology, 2009, v. 30 n. 1, p. 127-135 How to Cite?
AbstractHuman neuroblastoma SH-SY5Y is a dopaminergic neuronal cell line which has been used as an in vitro model for neurotoxicity experiments. Although the neuroblastoma is usually differentiated by all-trans-retinoic acid (RA), both RA-differentiated and undifferentiated SH-SY5Y cells have been used in neuroscience research. However, the changes in neuronal properties triggered by RA as well as the subsequent responsiveness to neurotoxins have not been comprehensively studied. Therefore, we aim to re-evaluate the differentiation property of RA on this cell line. We hypothesize that modulation of signaling pathways and neuronal properties during RA-mediated differentiation in SH-SY5Y cells can affect their susceptibility to neurotoxins. The differentiation property of RA was confirmed by showing an extensive outgrowth of neurites, increased expressions of neuronal nuclei, neuron specific enolase, synaptophysin and synaptic associated protein-97, and decreased expression of inhibitor of differentiation-1. While undifferentiated SH-SY5Y cells were susceptible to 6-OHDA and MPP+, RA-differentiation conferred SH-SY5Y cells higher tolerance, potentially by up-regulating survival signaling, including Akt pathway as inhibition of Akt removed RA-induced neuroprotection against 6-OHDA. As a result, the real toxicity cannot be revealed in RA-differentiated cells. Therefore, undifferentiated SH-SY5Y is more appropriate for studying neurotoxicity or neuroprotection in experimental Parkinson's disease research. © 2008 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/58226
ISSN
2015 Impact Factor: 2.738
2015 SCImago Journal Rankings: 1.245
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant Council, Hong Kong7552/06M
N-HKU 707/07 M
University of Hong Kong
HKU Seed200711159028
Funding Information:

This work is supported by competitive earmarked research grant (7552/06M) and NSFC/RGC Joint Research Scheme (N-HKU 707/07 M) from Research Grant Council, Hong Kong, University Strategic Research Theme on Drug Discovery from The University of Hong Kong, and HKU Seed Funding for Basic Research (200711159028).

References

 

DC FieldValueLanguage
dc.contributor.authorCheung, YTen_HK
dc.contributor.authorLau, WKWen_HK
dc.contributor.authorYu, MSen_HK
dc.contributor.authorLai, CSWen_HK
dc.contributor.authorYeung, SCen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorChang, RCCen_HK
dc.date.accessioned2010-05-31T03:26:11Z-
dc.date.available2010-05-31T03:26:11Z-
dc.date.issued2009en_HK
dc.identifier.citationNeurotoxicology, 2009, v. 30 n. 1, p. 127-135en_HK
dc.identifier.issn0161-813Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/58226-
dc.description.abstractHuman neuroblastoma SH-SY5Y is a dopaminergic neuronal cell line which has been used as an in vitro model for neurotoxicity experiments. Although the neuroblastoma is usually differentiated by all-trans-retinoic acid (RA), both RA-differentiated and undifferentiated SH-SY5Y cells have been used in neuroscience research. However, the changes in neuronal properties triggered by RA as well as the subsequent responsiveness to neurotoxins have not been comprehensively studied. Therefore, we aim to re-evaluate the differentiation property of RA on this cell line. We hypothesize that modulation of signaling pathways and neuronal properties during RA-mediated differentiation in SH-SY5Y cells can affect their susceptibility to neurotoxins. The differentiation property of RA was confirmed by showing an extensive outgrowth of neurites, increased expressions of neuronal nuclei, neuron specific enolase, synaptophysin and synaptic associated protein-97, and decreased expression of inhibitor of differentiation-1. While undifferentiated SH-SY5Y cells were susceptible to 6-OHDA and MPP+, RA-differentiation conferred SH-SY5Y cells higher tolerance, potentially by up-regulating survival signaling, including Akt pathway as inhibition of Akt removed RA-induced neuroprotection against 6-OHDA. As a result, the real toxicity cannot be revealed in RA-differentiated cells. Therefore, undifferentiated SH-SY5Y is more appropriate for studying neurotoxicity or neuroprotection in experimental Parkinson's disease research. © 2008 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroen_HK
dc.relation.ispartofNeuroToxicologyen_HK
dc.rightsNeuroToxicology. Copyright © Elsevier BV.en_HK
dc.subject.mesh1-Methyl-4-phenylpyridinium - toxicityen_HK
dc.subject.meshBiological Markers - analysisen_HK
dc.subject.meshCell Differentiation - drug effectsen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshHumansen_HK
dc.subject.meshModels, Neurologicalen_HK
dc.subject.meshNeuroblastomaen_HK
dc.subject.meshNeurons - drug effectsen_HK
dc.subject.meshOxidopamine - toxicityen_HK
dc.subject.meshReactive Oxygen Species - metabolismen_HK
dc.subject.meshSignal Transductionen_HK
dc.subject.meshTretinoin - pharmacologyen_HK
dc.titleEffects of all-trans-retinoic acid on human SH-SY5Y neuroblastoma as in vitro model in neurotoxicity researchen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0161-813X&volume=30&spage=127&epage=135&date=2009&atitle=Effects+of+all-trans-retinoic+acid+on+human+SH-SY5Y+neuroblastoma+as+in+vitro+model+in+neurotoxicity+researchen_HK
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.doi10.1016/j.neuro.2008.11.001en_HK
dc.identifier.pmid19056420-
dc.identifier.scopuseid_2-s2.0-58749087320en_HK
dc.identifier.hkuros154884en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-58749087320&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume30en_HK
dc.identifier.issue1en_HK
dc.identifier.spage127en_HK
dc.identifier.epage135en_HK
dc.identifier.isiWOS:000263047400017-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridCheung, YT=16678256500en_HK
dc.identifier.scopusauthoridLau, WKW=35292424400en_HK
dc.identifier.scopusauthoridYu, MS=35346047600en_HK
dc.identifier.scopusauthoridLai, CSW=26022547000en_HK
dc.identifier.scopusauthoridYeung, SC=25923636600en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.scopusauthoridChang, RCC=7403713410en_HK

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