Article: A DEAB-sensitive aldehyde dehydrogenase regulates hematopoietic stem and progenitor cells development during primitive hematopoiesis in zebrafish embryos

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TitleA DEAB-sensitive aldehyde dehydrogenase regulates hematopoietic stem and progenitor cells development during primitive hematopoiesis in zebrafish embryos
AuthorsMa, ACH1
Chung, MIS1
Liang, R1
Leung, AYH1
Issue Date2010
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/leu
CitationLeukemia, 2010, v. 24 n. 12, p. 2090-2099 [How to Cite?]
DOI: http://dx.doi.org/10.1038/leu.2010.206
AbstractAlthough aldehyde dehydrogenase (ALDH) activity has become a surrogate of hematopoietic stem and progenitor cells (HSPCs), its function during hematopoiesis was unclear. Here, we examined its role in zebrafish hematopoiesis based on pharmacological inhibition and morpholino (MO) knockdown. Zebrafish embryos were treated with diethylaminobenzaldehyde (DEAB, 1 mol/l) between 0- and 48 hour-post-fertilization (hpf). MOs targeting aldhs were injected between 1 and 4-cell stage. The effects on hematopoiesis were evaluated at different stages. DEAB treatment between 0 and 18 hpf increased gene expression associated with HSPC (scl, lmo2), erythropoiesis (gata1, α- and Β-eHb) and myelopoiesis (spi1) as well as gfp cells in dissociated Tg(gata1:gfp) embryos. The effects were ameliorated by all-trans retinoic acid (1 nmol/l). Definitive hematopoiesis and the erythromyeloid precursors were unaffected. In all, 14 out of 15 zebrafish aldhs were detectable by reverse transcription PCR in 18 hpf embryos, of which only aldh1a2 and aldh16a1 were expressed in sites pertinent to hematopoiesis. Molecular targeting by MOs was demonstrated for 15 aldhs, but none of them, even in combined aldh1a2 and aldh1a3 knockdown, recapitulated the hematopoietic expansion in DEAB-treated embryos. In conclusion, DEAB expands HSPC population during primitive hematopoiesis through inhibition of aldh and retinoic acid synthesis. The specific aldh isoform(s) remains to be determined. © 2010 Macmillan Publishers Limited All rights reserved.
ISSN0887-6924
2011 Impact Factor: 9.561
2011 SCImago Journal Rankings: 1.237
DOIhttp://dx.doi.org/10.1038/leu.2010.206
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorMa, ACH
dc.contributor.authorChung, MIS
dc.contributor.authorLiang, R
dc.contributor.authorLeung, AYH
dc.date.accessioned2012-09-05T05:30:25Z
dc.date.available2012-09-05T05:30:25Z
dc.date.issued2010
dc.description.abstractAlthough aldehyde dehydrogenase (ALDH) activity has become a surrogate of hematopoietic stem and progenitor cells (HSPCs), its function during hematopoiesis was unclear. Here, we examined its role in zebrafish hematopoiesis based on pharmacological inhibition and morpholino (MO) knockdown. Zebrafish embryos were treated with diethylaminobenzaldehyde (DEAB, 1 mol/l) between 0- and 48 hour-post-fertilization (hpf). MOs targeting aldhs were injected between 1 and 4-cell stage. The effects on hematopoiesis were evaluated at different stages. DEAB treatment between 0 and 18 hpf increased gene expression associated with HSPC (scl, lmo2), erythropoiesis (gata1, α- and Β-eHb) and myelopoiesis (spi1) as well as gfp cells in dissociated Tg(gata1:gfp) embryos. The effects were ameliorated by all-trans retinoic acid (1 nmol/l). Definitive hematopoiesis and the erythromyeloid precursors were unaffected. In all, 14 out of 15 zebrafish aldhs were detectable by reverse transcription PCR in 18 hpf embryos, of which only aldh1a2 and aldh16a1 were expressed in sites pertinent to hematopoiesis. Molecular targeting by MOs was demonstrated for 15 aldhs, but none of them, even in combined aldh1a2 and aldh1a3 knockdown, recapitulated the hematopoietic expansion in DEAB-treated embryos. In conclusion, DEAB expands HSPC population during primitive hematopoiesis through inhibition of aldh and retinoic acid synthesis. The specific aldh isoform(s) remains to be determined. © 2010 Macmillan Publishers Limited All rights reserved.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationLeukemia, 2010, v. 24 n. 12, p. 2090-2099 [How to Cite?]
DOI: http://dx.doi.org/10.1038/leu.2010.206
dc.identifier.citeulike7967680
dc.identifier.doihttp://dx.doi.org/10.1038/leu.2010.206
dc.identifier.epage2099
dc.identifier.issn0887-6924
2011 Impact Factor: 9.561
2011 SCImago Journal Rankings: 1.237
dc.identifier.issue12
dc.identifier.pmid20927131
dc.identifier.scopuseid_2-s2.0-78650304777
dc.identifier.spage2090
dc.identifier.urihttp://hdl.handle.net/10722/163350
dc.identifier.volume24
dc.languageeng
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/leu
dc.publisher.placeUnited Kingdom
dc.relation.ispartofLeukemia
dc.relation.referencesReferences in Scopus
dc.subject.meshAldehyde Dehydrogenase - Antagonists & Inhibitors - Physiology
dc.subject.meshAnimals
dc.subject.meshCell Differentiation - Drug Effects
dc.subject.meshEnzyme Inhibitors - Pharmacology
dc.subject.meshGene Expression Profiling
dc.subject.meshGene Expression Regulation, Developmental - Drug Effects
dc.subject.meshHematopoiesis - Drug Effects
dc.subject.meshHematopoietic Stem Cells - Drug Effects - Physiology
dc.subject.meshTretinoin - Pharmacology
dc.subject.meshZebrafish - Embryology
dc.titleA DEAB-sensitive aldehyde dehydrogenase regulates hematopoietic stem and progenitor cells development during primitive hematopoiesis in zebrafish embryos
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong