File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Cyp26b1 mediates differential neurogenicity in axial-specific populations of adult spinal cord progenitor cells

TitleCyp26b1 mediates differential neurogenicity in axial-specific populations of adult spinal cord progenitor cells
Authors
KeywordsRetinal dehydrogenase
Retinoic acid
Animal cell
Cervical spinal cord
Gene expression
Issue Date2012
PublisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/jht
Citation
Stem Cells and Development, 2012, v. 21 n. 12, p. 2252-2261 How to Cite?
AbstractUtilization of endogenous adult spinal cord progenitor cells (SCPCs) for neuronal regeneration is a promising strategy for spinal cord repair. To mobilize endogenous SCPCs for injury repair, it is necessary to understand their intrinsic properties and to identify signaling factors that can stimulate their neurogenic potential. In this study, we demonstrate that adult mouse SCPCs express distinct combinatorial Hox genes and exhibit axial-specific stem cell properties. Lumbar-derived neurospheres displayed higher primary sphere formation and greater neurogenicity compared with cervical- and thoracic-derived neurospheres. To further understand the mechanisms governing neuronal differentiation of SCPCs from specific axial regions, we examined the neurogenic responses of adult SCPCs to retinoic acid (RA), an essential factor for adult neurogenesis. Although RA is a potent inducer of neuronal differentiation, we found that RA enhanced the generation of neurons specifically in cervical- but not lumbar-derived cells. We further demonstrate that the differential RA response was mediated by the RA-degrading enzyme cytochrome P450 oxidase b1 Cyp26b1. Lumbar cells express high levels of Cyp26b1 and low levels of the RA-synthesizing enzyme retinaldehyde dehydrogenase Raldh2, resulting in limited activation of the RA signaling pathway in these cells. In contrast, low Cyp26b1 expression in cervical spinal cord progenitor cells allows RA signaling to be readily activated upon RA treatment. The intrinsic heterogeneity and signaling factor regulation among adult SCPCs suggest that different niche factor regimens are required for site-specific mobilization of endogenous SCPCs from distinct spatial regions of the spinal cord for injury repair.
Persistent Identifierhttp://hdl.handle.net/10722/149060
ISSN
2015 Impact Factor: 3.777
2015 SCImago Journal Rankings: 1.703
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLeung, Cen_US
dc.contributor.authorChan, SCLen_US
dc.contributor.authorTsang, SLen_US
dc.contributor.authorWu, Wen_US
dc.contributor.authorSham, MHen_US
dc.date.accessioned2012-06-22T06:19:25Z-
dc.date.available2012-06-22T06:19:25Z-
dc.date.issued2012en_US
dc.identifier.citationStem Cells and Development, 2012, v. 21 n. 12, p. 2252-2261en_US
dc.identifier.issn1547-3287-
dc.identifier.urihttp://hdl.handle.net/10722/149060-
dc.description.abstractUtilization of endogenous adult spinal cord progenitor cells (SCPCs) for neuronal regeneration is a promising strategy for spinal cord repair. To mobilize endogenous SCPCs for injury repair, it is necessary to understand their intrinsic properties and to identify signaling factors that can stimulate their neurogenic potential. In this study, we demonstrate that adult mouse SCPCs express distinct combinatorial Hox genes and exhibit axial-specific stem cell properties. Lumbar-derived neurospheres displayed higher primary sphere formation and greater neurogenicity compared with cervical- and thoracic-derived neurospheres. To further understand the mechanisms governing neuronal differentiation of SCPCs from specific axial regions, we examined the neurogenic responses of adult SCPCs to retinoic acid (RA), an essential factor for adult neurogenesis. Although RA is a potent inducer of neuronal differentiation, we found that RA enhanced the generation of neurons specifically in cervical- but not lumbar-derived cells. We further demonstrate that the differential RA response was mediated by the RA-degrading enzyme cytochrome P450 oxidase b1 Cyp26b1. Lumbar cells express high levels of Cyp26b1 and low levels of the RA-synthesizing enzyme retinaldehyde dehydrogenase Raldh2, resulting in limited activation of the RA signaling pathway in these cells. In contrast, low Cyp26b1 expression in cervical spinal cord progenitor cells allows RA signaling to be readily activated upon RA treatment. The intrinsic heterogeneity and signaling factor regulation among adult SCPCs suggest that different niche factor regimens are required for site-specific mobilization of endogenous SCPCs from distinct spatial regions of the spinal cord for injury repair.-
dc.languageengen_US
dc.publisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/jht-
dc.relation.ispartofStem Cells and Developmenten_US
dc.rightsThis is a copy of an article published in the [Stem Cells and Development] © [2012] [copyright Mary Ann Liebert, Inc.]; [Stem Cells and Development} is available online at: http://www.liebertonline.com.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectRetinal dehydrogenase-
dc.subjectRetinoic acid-
dc.subjectAnimal cell-
dc.subjectCervical spinal cord-
dc.subjectGene expression-
dc.titleCyp26b1 mediates differential neurogenicity in axial-specific populations of adult spinal cord progenitor cellsen_US
dc.typeArticleen_US
dc.identifier.emailLeung, C: leungcar@hkucc.hku.hken_US
dc.identifier.emailTsang, SL: sltsang@hku.hken_US
dc.identifier.emailWu, W: wtwu@hkucc.hku.hken_US
dc.identifier.emailSham, MH: mhsham@hku.hken_US
dc.identifier.authorityWu, W=rp00419en_US
dc.identifier.authoritySham, MH=rp00380en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1089/scd.2011.0613-
dc.identifier.pmid22214285-
dc.identifier.scopuseid_2-s2.0-84863277831-
dc.identifier.hkuros200417en_US
dc.identifier.volume21en_US
dc.identifier.issue12-
dc.identifier.spage2252-
dc.identifier.epage2261-
dc.identifier.eissn1557-8534-
dc.identifier.isiWOS:000307295500016-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats