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Article: Alteration in the expression of bone morphogenetic protein-2,3,4,5 mRNA during pathogenesis of cleft palate in BALB/c mice

TitleAlteration in the expression of bone morphogenetic protein-2,3,4,5 mRNA during pathogenesis of cleft palate in BALB/c mice
Authors
Issue Date2000
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/archoralbio
Citation
Archives Of Oral Biology, 2000, v. 45 n. 2, p. 133-140 How to Cite?
AbstractTo identify the function of these bone morphogenetic proteins (BMP) during pathogenesis of cleft palate, an experimental model was established in BALB/c mice. Cleft palate was induced by exposure to retinoic acid on embryonic day (E)12. The expression of BMP-2,3,4,5 mRNA in normal and abnormal embryonic palatal shelves was then examined from E13 to E16 by in situ hybridization. The results showed that BMP-4 mRNA was expressed strongly and uniformly in normal epithelial cells and dispersed mesenchymal cells on E13. BMP-2,5 mRNA expression appeared only in dispersed mesenchymal cells. With the development of shelves, the staining density of BMP-2,4,5 decreased gradually in mesenchymal cells outside of the condensation and increased inside the condensation. After shelves had fused on E16, no positive signals for BMP-2,4,5 were detected in dispersed mesenchymal cells, but their expression persisted in the condensation. Exposure to retinoic acid delayed the formation of the condensation and decreased BMP-2,4,5 mRNA dramatically in mesenchyme from E13 to E15. BMP-3 mRNA expression were almost negative in either control or retinoic acid-treated groups during all stages. It was concluded that spatial and temporal expression of BMP-2,4,5 was required during normal palatogenesis, and that a deficiency of their mRNA expression may contribute to the pathogenesis of cleft palate. (C) 2000 Elsevier Science Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/67984
ISSN
2015 Impact Factor: 1.733
2015 SCImago Journal Rankings: 0.713
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLu, Hen_HK
dc.contributor.authorJin, Yen_HK
dc.contributor.authorTipoe, GLen_HK
dc.date.accessioned2010-09-06T06:00:04Z-
dc.date.available2010-09-06T06:00:04Z-
dc.date.issued2000en_HK
dc.identifier.citationArchives Of Oral Biology, 2000, v. 45 n. 2, p. 133-140en_HK
dc.identifier.issn0003-9969en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67984-
dc.description.abstractTo identify the function of these bone morphogenetic proteins (BMP) during pathogenesis of cleft palate, an experimental model was established in BALB/c mice. Cleft palate was induced by exposure to retinoic acid on embryonic day (E)12. The expression of BMP-2,3,4,5 mRNA in normal and abnormal embryonic palatal shelves was then examined from E13 to E16 by in situ hybridization. The results showed that BMP-4 mRNA was expressed strongly and uniformly in normal epithelial cells and dispersed mesenchymal cells on E13. BMP-2,5 mRNA expression appeared only in dispersed mesenchymal cells. With the development of shelves, the staining density of BMP-2,4,5 decreased gradually in mesenchymal cells outside of the condensation and increased inside the condensation. After shelves had fused on E16, no positive signals for BMP-2,4,5 were detected in dispersed mesenchymal cells, but their expression persisted in the condensation. Exposure to retinoic acid delayed the formation of the condensation and decreased BMP-2,4,5 mRNA dramatically in mesenchyme from E13 to E15. BMP-3 mRNA expression were almost negative in either control or retinoic acid-treated groups during all stages. It was concluded that spatial and temporal expression of BMP-2,4,5 was required during normal palatogenesis, and that a deficiency of their mRNA expression may contribute to the pathogenesis of cleft palate. (C) 2000 Elsevier Science Ltd.en_HK
dc.languageengen_HK
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/archoralbioen_HK
dc.relation.ispartofArchives of Oral Biologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBone Morphogenetic Protein 2en_HK
dc.subject.meshBone Morphogenetic Protein 3en_HK
dc.subject.meshBone Morphogenetic Protein 4en_HK
dc.subject.meshBone Morphogenetic Protein 5en_HK
dc.subject.meshBone Morphogenetic Proteins - geneticsen_HK
dc.subject.meshCleft Palate - embryology - geneticsen_HK
dc.subject.meshColoring Agents - diagnostic useen_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshEpithelial Cells - drug effects - metabolismen_HK
dc.subject.meshGene Expression Regulationen_HK
dc.subject.meshGrowth Substances - geneticsen_HK
dc.subject.meshIn Situ Hybridizationen_HK
dc.subject.meshMesoderm - drug effects - metabolism - pathologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred BALB Cen_HK
dc.subject.meshPalate - drug effects - embryologyen_HK
dc.subject.meshRNA, Messenger - geneticsen_HK
dc.subject.meshTransforming Growth Factor beta - geneticsen_HK
dc.subject.meshTretinoin - adverse effectsen_HK
dc.titleAlteration in the expression of bone morphogenetic protein-2,3,4,5 mRNA during pathogenesis of cleft palate in BALB/c miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0003-9969&volume=45&spage=133&epage=140&date=2000&atitle=Alteration+in+the+expression+of+bone+morphogenetic+protein-2,3,4,5+mRNA+during+pathogenesis+of+cleft+palate+in+BALB/c+miceen_HK
dc.identifier.emailTipoe, GL:tgeorge@hkucc.hku.hken_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0003-9969(99)00118-1en_HK
dc.identifier.pmid10716617-
dc.identifier.scopuseid_2-s2.0-0034141886en_HK
dc.identifier.hkuros49620en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034141886&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume45en_HK
dc.identifier.issue2en_HK
dc.identifier.spage133en_HK
dc.identifier.epage140en_HK
dc.identifier.isiWOS:000085402500004-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLu, H=7404843896en_HK
dc.identifier.scopusauthoridJin, Y=26643271200en_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK

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