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</script>doi: 10.1139/o10-013
pmid: 20651846
Cleft lip and cleft palate are common congenital craniofacial birth defects in humans. Phenytoin (PHT) is a risk factor of cleft palate formation; however, the molecular mechanisms by which phenytoin exerts its teratogenic effects resulting in cleft palate remain unknown. The Satb2 gene mutation is associated with cleft palate. Satb2-deficient mice exhibit cleft palate deformity and an up-regulation of Hoxa2 in the fronto-nasal region. In this study, phenytoin was administered intraperitoneally to pregnant C57BL/6 mice on the 10th day of gestation. Real-time PCR results showed that the expressions of Satb2 and Hoxa2 in craniofacial tissues of mouse embryos were obviously different at different time points. The Satb2 gene was down-regulated and the Hoxa2 gene was up-regulated in phenytoin-treated mouse embryonic craniofacial tissue. We conclude that phenytoin may regulate the expression of these two genes in C57BL/6 mice and it may also be involved in the formation of cleft palate.
Homeodomain Proteins, Cleft Lip, Skull, Gene Expression Regulation, Developmental, Matrix Attachment Region Binding Proteins, Embryo, Mammalian, Cleft Palate, Mice, Inbred C57BL, Mice, Fetus, Pregnancy, Face, Phenytoin, Animals, Anticonvulsants, Female, Maxillofacial Development, Transcription Factors
Homeodomain Proteins, Cleft Lip, Skull, Gene Expression Regulation, Developmental, Matrix Attachment Region Binding Proteins, Embryo, Mammalian, Cleft Palate, Mice, Inbred C57BL, Mice, Fetus, Pregnancy, Face, Phenytoin, Animals, Anticonvulsants, Female, Maxillofacial Development, Transcription Factors
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