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Article: A critical role of Pax6 in alcohol-induced fetal microcephaly

TitleA critical role of Pax6 in alcohol-induced fetal microcephaly
Authors
KeywordsFAS
Fetal alcohol syndrome
fetal alcohol syndrome
Microcephaly
MMR
Modified Marc's Ringer
Pax6
Reactive oxygen species
reactive oxygen species
ROS
Issue Date2004
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ynbdi
Citation
Neurobiology Of Disease, 2004, v. 16 n. 2, p. 370-376 How to Cite?
AbstractMaternal alcohol abuse during pregnancy is one of the leading causes of birth defects in humans. Despite extensive studies, the molecular basis is still not clear. Here we transiently exposed Xenopus embryos to alcohol and showed that alcohol dose-dependently produced microcephaly and growth retardation. Moreover, it reduced the expression of several key neural genes (xPax6, xOtx2, xSox3, xSox2, and xNCAM), of which xPax6 was most vulnerable. An alcohol concentration as low as 0.3% could produce more than 90% reduction of xPax6 expression. Consistently, microinjection of xPax6 expression plasmid to Xenopus embryos dose-dependently rescued alcohol-induced microcephaly and restored the expression of xOtx2, xSox3, xSox2, and xNCAM. To test whether reactive oxygen species (ROS) is the upstream signal for alcohol-induced microcephaly and xPax6 suppression, we overexpressed catalase in Xenopus embryos and found that catalase not only decreased alcohol-induced H 2O 2 formation, but also fully restored Pax6 expression and reversed microcephaly. In contrast, xPax6 and catalase could only provide partial protection against growth retardation. Results from this study illustrate for the first time the critical role of H 2O 2-mediated Pax6 suppression in alcohol-induced microcephaly and suggest the presence of additional mechanisms for alcohol-induced fetal growth retardation. © 2004 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/87987
ISSN
2015 Impact Factor: 4.856
2015 SCImago Journal Rankings: 2.875
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPeng, Yen_HK
dc.contributor.authorYang, PHen_HK
dc.contributor.authorNg, SSMen_HK
dc.contributor.authorWong, OGen_HK
dc.contributor.authorLiu, Jen_HK
dc.contributor.authorHe, MLen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorLin, MCMen_HK
dc.date.accessioned2010-09-06T09:37:10Z-
dc.date.available2010-09-06T09:37:10Z-
dc.date.issued2004en_HK
dc.identifier.citationNeurobiology Of Disease, 2004, v. 16 n. 2, p. 370-376en_HK
dc.identifier.issn0969-9961en_HK
dc.identifier.urihttp://hdl.handle.net/10722/87987-
dc.description.abstractMaternal alcohol abuse during pregnancy is one of the leading causes of birth defects in humans. Despite extensive studies, the molecular basis is still not clear. Here we transiently exposed Xenopus embryos to alcohol and showed that alcohol dose-dependently produced microcephaly and growth retardation. Moreover, it reduced the expression of several key neural genes (xPax6, xOtx2, xSox3, xSox2, and xNCAM), of which xPax6 was most vulnerable. An alcohol concentration as low as 0.3% could produce more than 90% reduction of xPax6 expression. Consistently, microinjection of xPax6 expression plasmid to Xenopus embryos dose-dependently rescued alcohol-induced microcephaly and restored the expression of xOtx2, xSox3, xSox2, and xNCAM. To test whether reactive oxygen species (ROS) is the upstream signal for alcohol-induced microcephaly and xPax6 suppression, we overexpressed catalase in Xenopus embryos and found that catalase not only decreased alcohol-induced H 2O 2 formation, but also fully restored Pax6 expression and reversed microcephaly. In contrast, xPax6 and catalase could only provide partial protection against growth retardation. Results from this study illustrate for the first time the critical role of H 2O 2-mediated Pax6 suppression in alcohol-induced microcephaly and suggest the presence of additional mechanisms for alcohol-induced fetal growth retardation. © 2004 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ynbdien_HK
dc.relation.ispartofNeurobiology of Diseaseen_HK
dc.subjectFASen_HK
dc.subjectFetal alcohol syndromeen_HK
dc.subjectfetal alcohol syndromeen_HK
dc.subjectMicrocephalyen_HK
dc.subjectMMRen_HK
dc.subjectModified Marc's Ringeren_HK
dc.subjectPax6en_HK
dc.subjectReactive oxygen speciesen_HK
dc.subjectreactive oxygen speciesen_HK
dc.subjectROSen_HK
dc.titleA critical role of Pax6 in alcohol-induced fetal microcephalyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0969-9961&volume=16&spage=370&epage=376&date=2004&atitle=A+critical+role+of+Pax6+in+alcohol-induced+fetal+microcephalyen_HK
dc.identifier.emailNg, SSM: ssmng@hku.hken_HK
dc.identifier.emailLin, MCM: mcllin@hkucc.hku.hken_HK
dc.identifier.authorityNg, SSM=rp00767en_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.nbd.2004.03.004en_HK
dc.identifier.pmid15193293-
dc.identifier.scopuseid_2-s2.0-2942527145en_HK
dc.identifier.hkuros91807en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-2942527145&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume16en_HK
dc.identifier.issue2en_HK
dc.identifier.spage370en_HK
dc.identifier.epage376en_HK
dc.identifier.isiWOS:000222093400008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridPeng, Y=7403419265en_HK
dc.identifier.scopusauthoridYang, PH=24340289000en_HK
dc.identifier.scopusauthoridNg, SSM=7403358718en_HK
dc.identifier.scopusauthoridWong, OG=7004813981en_HK
dc.identifier.scopusauthoridLiu, J=36014680100en_HK
dc.identifier.scopusauthoridHe, ML=35080389700en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK

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