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Article: MiR-200b is involved in Tgf-β signaling to regulate mammalian palate development

TitleMiR-200b is involved in Tgf-β signaling to regulate mammalian palate development
Authors
Issue Date2012
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00418/index.htm
Citation
Histochemistry And Cell Biology, 2012, v. 137 n. 1, p. 67-78 How to Cite?
AbstractVarious cellular and molecular events are involved in palatogenesis, including apoptosis, epithelial- mesenchymal transition (EMT), cell proliferation, and cell migration. Smad2 and Snail, which are well-known key mediators of the transforming growth factor beta (Tgf-β) pathway, play a crucial role in the regulation of palate development. Regulatory effects of microRNA 200b (miR- 200b) on Smad2 and Snail in palatogenesis have not yet been elucidated. The aim of this study is to determine the relationship between palate development regulators miR-200b and Tgf-β-mediated genes. Expression of miR-200b, E-cadherin, Smad2, and Snail was detected in the mesenchyme of the mouse palate, while miR-200b was expressed in the medial edge epithelium (MEE) and palatal mesenchyme. After the contact of palatal shelves, miR- 200b was no longer expressed in the mesenchyme around the fusion region. The binding activity of miR-200b to both Smad2 and Snail was examined using a luciferase assay. MiR-200b directly targeted Smad2 and Snail at both cellular and molecular levels. The function of miR-200b was determined by overexpression via a lentiviral vector in the palatal shelves. Ectopic expression of miR-200b resulted in suppression of these Tgf-β-mediated regulators and changes of apoptosis and cell proliferation in the palatal fusion region. These results suggest that miR-200b plays a crucial role in regulating the Smad2, Snail, and in apoptosis during palatogenesis by acting as a direct non-coding, influencing factor. Furthermore, the molecular interactions between miR-200b and Tgf-β signaling are important for proper palatogenesis and especially for palate fusion. Elucidating the mechanism of palatogenesis may aid the design of effective gene-based therapies for the treatment of congenital cleft palate. © Springer-Verlag 2011.
Persistent Identifierhttp://hdl.handle.net/10722/169589
ISSN
2015 Impact Factor: 2.78
2015 SCImago Journal Rankings: 1.287
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShin, JOen_US
dc.contributor.authorLee, JMen_US
dc.contributor.authorCho, KWen_US
dc.contributor.authorKwak, Sen_US
dc.contributor.authorKwon, HJen_US
dc.contributor.authorLee, MJen_US
dc.contributor.authorCho, SWen_US
dc.contributor.authorKim, KSen_US
dc.contributor.authorJung, HSen_US
dc.date.accessioned2012-10-25T04:53:13Z-
dc.date.available2012-10-25T04:53:13Z-
dc.date.issued2012en_US
dc.identifier.citationHistochemistry And Cell Biology, 2012, v. 137 n. 1, p. 67-78en_US
dc.identifier.issn0948-6143en_US
dc.identifier.urihttp://hdl.handle.net/10722/169589-
dc.description.abstractVarious cellular and molecular events are involved in palatogenesis, including apoptosis, epithelial- mesenchymal transition (EMT), cell proliferation, and cell migration. Smad2 and Snail, which are well-known key mediators of the transforming growth factor beta (Tgf-β) pathway, play a crucial role in the regulation of palate development. Regulatory effects of microRNA 200b (miR- 200b) on Smad2 and Snail in palatogenesis have not yet been elucidated. The aim of this study is to determine the relationship between palate development regulators miR-200b and Tgf-β-mediated genes. Expression of miR-200b, E-cadherin, Smad2, and Snail was detected in the mesenchyme of the mouse palate, while miR-200b was expressed in the medial edge epithelium (MEE) and palatal mesenchyme. After the contact of palatal shelves, miR- 200b was no longer expressed in the mesenchyme around the fusion region. The binding activity of miR-200b to both Smad2 and Snail was examined using a luciferase assay. MiR-200b directly targeted Smad2 and Snail at both cellular and molecular levels. The function of miR-200b was determined by overexpression via a lentiviral vector in the palatal shelves. Ectopic expression of miR-200b resulted in suppression of these Tgf-β-mediated regulators and changes of apoptosis and cell proliferation in the palatal fusion region. These results suggest that miR-200b plays a crucial role in regulating the Smad2, Snail, and in apoptosis during palatogenesis by acting as a direct non-coding, influencing factor. Furthermore, the molecular interactions between miR-200b and Tgf-β signaling are important for proper palatogenesis and especially for palate fusion. Elucidating the mechanism of palatogenesis may aid the design of effective gene-based therapies for the treatment of congenital cleft palate. © Springer-Verlag 2011.en_US
dc.languageengen_US
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00418/index.htmen_US
dc.relation.ispartofHistochemistry and Cell Biologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosisen_US
dc.subject.meshCadherins - Genetics - Metabolismen_US
dc.subject.meshCell Proliferationen_US
dc.subject.meshHek293 Cellsen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Icren_US
dc.subject.meshMicrornas - Genetics - Metabolismen_US
dc.subject.meshPalate - Cytology - Growth & Development - Metabolismen_US
dc.subject.meshReal-Time Polymerase Chain Reactionen_US
dc.subject.meshSignal Transduction - Geneticsen_US
dc.subject.meshSmad2 Protein - Genetics - Metabolismen_US
dc.subject.meshTranscription Factors - Genetics - Metabolismen_US
dc.subject.meshTransforming Growth Factor Beta - Genetics - Metabolismen_US
dc.titleMiR-200b is involved in Tgf-β signaling to regulate mammalian palate developmenten_US
dc.typeArticleen_US
dc.identifier.emailJung, HS: hsjung@yuhs.acen_US
dc.identifier.authorityJung, HS=rp01683en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s00418-011-0876-1en_US
dc.identifier.pmid22072420-
dc.identifier.scopuseid_2-s2.0-84857631069en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84857631069&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume137en_US
dc.identifier.issue1en_US
dc.identifier.spage67en_US
dc.identifier.epage78en_US
dc.identifier.isiWOS:000299380200006-
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridShin, JO=37361704500en_US
dc.identifier.scopusauthoridLee, JM=41361401200en_US
dc.identifier.scopusauthoridCho, KW=7403956665en_US
dc.identifier.scopusauthoridKwak, S=7202607781en_US
dc.identifier.scopusauthoridKwon, HJ=18836582500en_US
dc.identifier.scopusauthoridLee, MJ=36054770900en_US
dc.identifier.scopusauthoridCho, SW=32967447200en_US
dc.identifier.scopusauthoridKim, KS=52263802700en_US
dc.identifier.scopusauthoridJung, HS=7403030195en_US
dc.identifier.citeulike10037318-

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