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Article: The role of survivin in angiogenesis during zebrafish embryonic development

TitleThe role of survivin in angiogenesis during zebrafish embryonic development
Authors
Issue Date2007
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmcdevbiol/
Citation
Bmc Developmental Biology, 2007, v. 7 How to Cite?
AbstractBackground. Survivin is the smallest member of the inhibitor of apoptosis (IAP) gene family. Recently, the zebrafish survivin-1 gene has been cloned, showing remarkable sequence identity and similarity over the BIR domain compared with human and mouse survivin gene. Here we investigated the role of survivin in angiogenesis during zebrafish development. Morpholinos (MOs) targeting the 5′ untranslated region (UTR) (SurUTR) and sequences flanking the initiation codon (SurATG) of zebrafish survivin-1 gene were injected into embryos at 1-4 cell stage. Vasculature was examined by microangiography and GFP expression in Tg(fli1:EGFP)y1 embryos. Results: In embryos co-injected with SurUTR and Sur ATG-MOs, vasculogenesis was intact but angiogenesis was markedly perturbed, especially in the inter-segmental vessels (ISV) and dorsal longitudinal anastomotic vessels (DLAV) of the trunk, the inner optic circle and optic veins of developing eyes and the sub-intestinal vessels. Apoptosis was increased, as shown by TUNEL staining and increase in caspase-3 activity. Efficacy of SurUTR and SurATG-MOs was demonstrated by translation inhibition of co-injected 5′UTR survivin:GFP plasmids. The phenotypes could be recapitulated by splice-site MO targeting the exon2-intron junction of survivin gene and rescued by survivin mRNA. Injection of human vascular endothelial growth factor (VEGF) protein induced ectopic angiogenesis and increased survivin expression, whereas treatment with a VEGF receptor inhibitor markedly reduced angiogenesis and suppressed survivin expression. Conclusion: Survivin is involved in angiogenesis during zebrafish development and may be under VEGF regulation. © 2007 Ma et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/76412
ISSN
2020 Impact Factor: 1.978
2023 SCImago Journal Rankings: 0.736
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMa, ACHen_HK
dc.contributor.authorLin, Ren_HK
dc.contributor.authorChan, PKen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorMeng, Aen_HK
dc.contributor.authorVerfaillie, CMen_HK
dc.contributor.authorLiang, Ren_HK
dc.contributor.authorLeung, AYHen_HK
dc.date.accessioned2010-09-06T07:20:57Z-
dc.date.available2010-09-06T07:20:57Z-
dc.date.issued2007en_HK
dc.identifier.citationBmc Developmental Biology, 2007, v. 7en_HK
dc.identifier.issn1471-213Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/76412-
dc.description.abstractBackground. Survivin is the smallest member of the inhibitor of apoptosis (IAP) gene family. Recently, the zebrafish survivin-1 gene has been cloned, showing remarkable sequence identity and similarity over the BIR domain compared with human and mouse survivin gene. Here we investigated the role of survivin in angiogenesis during zebrafish development. Morpholinos (MOs) targeting the 5′ untranslated region (UTR) (SurUTR) and sequences flanking the initiation codon (SurATG) of zebrafish survivin-1 gene were injected into embryos at 1-4 cell stage. Vasculature was examined by microangiography and GFP expression in Tg(fli1:EGFP)y1 embryos. Results: In embryos co-injected with SurUTR and Sur ATG-MOs, vasculogenesis was intact but angiogenesis was markedly perturbed, especially in the inter-segmental vessels (ISV) and dorsal longitudinal anastomotic vessels (DLAV) of the trunk, the inner optic circle and optic veins of developing eyes and the sub-intestinal vessels. Apoptosis was increased, as shown by TUNEL staining and increase in caspase-3 activity. Efficacy of SurUTR and SurATG-MOs was demonstrated by translation inhibition of co-injected 5′UTR survivin:GFP plasmids. The phenotypes could be recapitulated by splice-site MO targeting the exon2-intron junction of survivin gene and rescued by survivin mRNA. Injection of human vascular endothelial growth factor (VEGF) protein induced ectopic angiogenesis and increased survivin expression, whereas treatment with a VEGF receptor inhibitor markedly reduced angiogenesis and suppressed survivin expression. Conclusion: Survivin is involved in angiogenesis during zebrafish development and may be under VEGF regulation. © 2007 Ma et al; licensee BioMed Central Ltd.en_HK
dc.languageengen_HK
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmcdevbiol/en_HK
dc.relation.ispartofBMC Developmental Biologyen_HK
dc.rightsB M C Developmental Biology. Copyright © BioMed Central Ltd.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshEmbryo, Nonmammalian - metabolismen_HK
dc.subject.meshGene Expression Regulation, Developmentalen_HK
dc.subject.meshInhibitor of Apoptosis Proteins - geneticsen_HK
dc.subject.meshNeovascularization, Physiologic - geneticsen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshVascular Endothelial Growth Factor A - geneticsen_HK
dc.subject.meshZebrafish - embryology - genetics - physiologyen_HK
dc.titleThe role of survivin in angiogenesis during zebrafish embryonic developmenten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1471-213X&volume=7&spage=50&epage=&date=2007&atitle=The+role+of+survivin+in+angiogenesis+during+zebrafish+embryonic+development.en_HK
dc.identifier.emailLeung, JCK:jckleung@hku.hken_HK
dc.identifier.emailLiang, R:rliang@hku.hken_HK
dc.identifier.emailLeung, AYH:ayhleung@hku.hken_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityLiang, R=rp00345en_HK
dc.identifier.authorityLeung, AYH=rp00265en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1186/1471-213X-7-50en_HK
dc.identifier.pmid17511868en_HK
dc.identifier.scopuseid_2-s2.0-34249825511en_HK
dc.identifier.hkuros137000en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34249825511&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume7en_HK
dc.identifier.isiWOS:000246805600001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridMa, ACH=15849157500en_HK
dc.identifier.scopusauthoridLin, R=16417180900en_HK
dc.identifier.scopusauthoridChan, PK=36944286400en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridChan, LYY=8108378300en_HK
dc.identifier.scopusauthoridMeng, A=7006106872en_HK
dc.identifier.scopusauthoridVerfaillie, CM=7004524257en_HK
dc.identifier.scopusauthoridLiang, R=26643224900en_HK
dc.identifier.scopusauthoridLeung, AYH=7403012668en_HK
dc.identifier.citeulike1308060-
dc.identifier.issnl1471-213X-

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