File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: Transcriptional profiling of enteric neural crest cells

TitleTranscriptional profiling of enteric neural crest cells
Authors
Issue Date2005
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/modo
Citation
15th International Society of Developmental Biologist Congress 2005, Sydney, Australia, 3-7 September 2005, In Mechanisms of Development, 2005, v. 122, Suppl. 1, p. S179, abstract no. 15-P016 How to Cite?
AbstractTo elucidate the molecular mechanisms mediating the stemness of neural crest cells (NCCs), we have isolated the NCCs from the mouse embryonic gut (E11.5) and cultured in form of neurospheres. The cultured NCCs are self-renewable and multipotent. RT-PCR analysis showed that they express various transcription factor genes characteristic of embryonic NCCs, including slug, snail, twist and Pax3. Nevertheless, the two master stemness regulators of embryonic stem cells, Nanog and Oct3/4, were not detected in the NCCs. Sonic hedgehog (Shh) was found to promote the proliferation and inhibit the glial cell line-derived neurotrophic factor (GDNF) induced differentiation of NCCs. With these mitogenic and neurotrophic factors, NCCs are fated to proliferate and differentiate, respectively. In attempt to study the transcriptional profiles of these fated NCCs, we have performed cDNA microarray analysis. Transcripts of 533 and 454 genes were changed in response to the GDNF and Shh treatments, respectively, when compared to the untreated control. They included neuronal markers, signaling, transcription/translation regulators, cell cycle related genes and expression sequence tag (EST) genes whose functions are unknown. In the subsequent data comparison study, we found that 50 genes, including 22% EST (11 genes), show opposite response to GDNF and Shh, of 2 to 24 folds difference at the transcriptional level. These genes may be implicated in the maintenance of the stemness of NCCs. Therefore, identification of the genes that govern proliferation and differentiation of NCCs would provide a means to reveal the stemness regulator(s) for NCCs.
DescriptionPoster abstract
Persistent Identifierhttp://hdl.handle.net/10722/96246
ISSN
2015 Impact Factor: 2.041
2015 SCImago Journal Rankings: 1.368

 

DC FieldValueLanguage
dc.contributor.authorNgan, ESWen_HK
dc.contributor.authorLui, VCHen_HK
dc.contributor.authorLau, KCen_HK
dc.contributor.authorGarcia-Barcelo, MMen_HK
dc.contributor.authorSham, MHen_HK
dc.contributor.authorTam, PKHen_HK
dc.date.accessioned2010-09-25T16:27:53Z-
dc.date.available2010-09-25T16:27:53Z-
dc.date.issued2005en_HK
dc.identifier.citation15th International Society of Developmental Biologist Congress 2005, Sydney, Australia, 3-7 September 2005, In Mechanisms of Development, 2005, v. 122, Suppl. 1, p. S179, abstract no. 15-P016-
dc.identifier.issn0925-4773-
dc.identifier.urihttp://hdl.handle.net/10722/96246-
dc.descriptionPoster abstract-
dc.description.abstractTo elucidate the molecular mechanisms mediating the stemness of neural crest cells (NCCs), we have isolated the NCCs from the mouse embryonic gut (E11.5) and cultured in form of neurospheres. The cultured NCCs are self-renewable and multipotent. RT-PCR analysis showed that they express various transcription factor genes characteristic of embryonic NCCs, including slug, snail, twist and Pax3. Nevertheless, the two master stemness regulators of embryonic stem cells, Nanog and Oct3/4, were not detected in the NCCs. Sonic hedgehog (Shh) was found to promote the proliferation and inhibit the glial cell line-derived neurotrophic factor (GDNF) induced differentiation of NCCs. With these mitogenic and neurotrophic factors, NCCs are fated to proliferate and differentiate, respectively. In attempt to study the transcriptional profiles of these fated NCCs, we have performed cDNA microarray analysis. Transcripts of 533 and 454 genes were changed in response to the GDNF and Shh treatments, respectively, when compared to the untreated control. They included neuronal markers, signaling, transcription/translation regulators, cell cycle related genes and expression sequence tag (EST) genes whose functions are unknown. In the subsequent data comparison study, we found that 50 genes, including 22% EST (11 genes), show opposite response to GDNF and Shh, of 2 to 24 folds difference at the transcriptional level. These genes may be implicated in the maintenance of the stemness of NCCs. Therefore, identification of the genes that govern proliferation and differentiation of NCCs would provide a means to reveal the stemness regulator(s) for NCCs.-
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/modo-
dc.relation.ispartofMechanisms of Developmenten_HK
dc.rightsMechanisms of Development. Copyright © Elsevier Ireland Ltd.-
dc.titleTranscriptional profiling of enteric neural crest cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailNgan, ESW: engan@hkucc.hku.hken_HK
dc.identifier.emailLui, VCH: vchlui@hkucc.hku.hken_HK
dc.identifier.emailGarcia-Barcelo, MM: mmgarcia@hkucc.hku.hken_HK
dc.identifier.emailSham, MH: mhsham@hkucc.hku.hken_HK
dc.identifier.emailTam, PKH: paultam@hkucc.hku.hken_HK
dc.identifier.authorityNgan, ESW=rp00422en_HK
dc.identifier.authorityLui, VCH=rp00363en_HK
dc.identifier.authorityGarcia-Barcelo, MM=rp00445en_HK
dc.identifier.authoritySham, MH=rp00380en_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.mod.2005.06.010-
dc.identifier.hkuros107110en_HK
dc.identifier.hkuros107079-
dc.identifier.volume122, Suppl. 1-
dc.identifier.spageS179-
dc.identifier.epageS179-
dc.publisher.placeIreland-
dc.description.other15th International Society of Developmental Biologist Congress 2005, Sydney, Australia, 3-7 September 2005, In Mechanisms of Development, 2005, v. 122, Suppl. 1, p. S179, abstract no. 15-P016-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats