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1.
Histochem Cell Biol ; 146(3): 289-300, 2016 Sep.
Article de Anglais | MEDLINE | ID: mdl-27166834

RÉSUMÉ

Intimate crosstalk occurs between the pulmonary epithelium and the vascular network during lung development. The transcription factor forkhead box f1 (Foxf1) is expressed in the lung mesenchyme and plays an indispensable role in pulmonary angiogenesis. Sonic hedgehog (Shh), a signalling molecule, is expressed in lung epithelium and is required to establish proper angiogenesis. It has been suggested that Foxf1, a downstream target of the Shh signalling pathway, mediates interaction between angiogenesis and the epithelium in lung. However, there has been no clear evidence showing the mechanism how Foxf1 is regulated by Shh signalling pathway during lung development. In this study, we investigated the lung-specific enhancers of Foxf1 and the Gli binding on the enhancers. At first, we found three evolutionarily conserved Foxf1 enhancers, two of which were long-range enhancers. Of the long-range enhancers, one demonstrated tissue-specific activity in the proximal and distal pulmonary blood vessels, while the other one demonstrated activity only in distal blood vessels. At analogous positions in human, these long-range enhancers were included in a regulatory region that was reportedly repeatedly deleted in alveolar capillary dysplasia with misalignment of pulmonary vein patients, which indicates the importance of these enhancers in pulmonary blood vessel formation. We also determined that Gli increased the activity of one of these long-range enhancers, which was specific to distal blood vessel, suggesting that Shh regulates Foxf1 transcription in pulmonary distal blood vessel formation.


Sujet(s)
Vaisseaux sanguins/métabolisme , Éléments activateurs (génétique)/génétique , Facteurs de transcription Forkhead/génétique , Veines pulmonaires/métabolisme , Transcription génétique , Animaux , Souris , Souris de lignée C57BL , Souris transgéniques , Analyse de séquence d'ADN
2.
Cell Tissue Res ; 341(2): 251-8, 2010 Aug.
Article de Anglais | MEDLINE | ID: mdl-20563598

RÉSUMÉ

Teeth, an excellent model for studying organogenesis, develop from a series of epithelial-mesenchymal interactions that are mediated by a complex molecular network. Bcor (BCL-6 interacting corepressor) has recently been discovered, but little is known about its function in tooth development. Mutations in BCOR affect humans with oculofaciocardiodental syndrome, which is an X-linked dominant disorder with presumed male lethality and which comprises microphthalmia, congenital cataracts, radiculomegaly, and cardiac and digital abnormalities. In this study, the Bcor expression pattern has been intensively investigated during mouse molar development. Bcor is expressed in both dental epithelium and the mesenchyme at E11.5. To understand the function of Bcor, knockdown of Bcor has been examined by using lentivirus-mediated RNA interference. Silencing of Bcor expression in dental mesenchymal cells at E14.5 causes dentinogenesis defects and retardation of tooth root development. Thus, our results suggest that Bcor expressed in the mesenchyme plays crucial roles during early tooth development. The function of Bcor expressed in the epithelium remains to be elucidated.


Sujet(s)
Mésoderme/embryologie , Odontogenèse , Protéines de répression/métabolisme , Dent/embryologie , Animaux , Régulation de l'expression des gènes au cours du développement , Humains , Lentivirus/génétique , Mâle , Mésoderme/métabolisme , Souris , Souris de lignée BALB C , Souris de lignée ICR , Odontogenèse/génétique , Interférence par ARN , Protéines de répression/antagonistes et inhibiteurs , Protéines de répression/génétique , Dent/métabolisme
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