Effect of Retinoic Acid on the Expression of PDGF Receptors During Palatogenesis / 대한해부학회지

Although cleft lip and palate are one of the most common craniofacial malformation, little is still known about the mechanism of the palate formation. Retinoic acid (RA) is known a teratogen, and cleft palate is induced by retinoic acid administration in the secondary palate formation stage. Many growth factors and their receptors are involved in the formation of the secondary palate. Here, we investigated the expression of PDGFR-alpha, and PDGFR-beta during palatogenesis after retinoid acid administration in mice by RT-PCR and immunohistochemistry. At E15.5, the opposing palatal shelves fused with one another in the control group, but the palatal shelves were not elevated and cleft palate was induced in the RA-treated group. In RT-PCR, PDGFR-beta was downregulated during palatogenesis after RA administration. In immunohistochemical experiment, PDGFR-alpha and PDGFR-beta were reduced in RA-induced group. Taken together, we suggest that PDGF receptors may be molecules involved in palate formation.

Effects of Maternal Hyperthermia on the Palatal Mesenchyme Development of Hsp70 Knock-out Mice Fetuses / 체질인류학회지

To investigate the effects of maternal hyperthermia on the development of the palate, pregnant Hsp70 knock-out mice at gestational day (GD) 8.5 were immersed in 43degrees C water bath until their body core temperature reached at 43degrees C. Thereafter, pregnant mice were given more 5 minutes hyperthermic exposure. Heat-untreated Hsp70 WT mice fetuses were used as the control group. Fetuses were collected at embryonic day 13.5, 14.5 and 15.5 (E13.5, E14, 5 and E15.5). Heads followed by removal of the mandible and the tongue were obtained and photographed for palatal development. Developing palates were processed for histological and immunohistochemical studies. Tissue sections were immunostained for TGF-beta2, FGF-8 and fibronectin, and observed with light microscope. The obtained results were as follows: Cleft palate was formed in heat-treated Hsp70 KO fetuses at E14.5 and E15.5. Immunohistochemical findings indicated that TGF-beta2 expression of the experimental fetuses were more delayed than that of the control fetuses. Mesenchyme under the medial edge epithelium (MEE) and cells of MEE showed continuously strong positive TGF-beta2 reactivity at E15.5. FGF-8 was revealed in both of the mesenchyme and the epithelium at the same time. FGF-8 immunoreactivity in the mesenchyme and the epithelium of the heat-treated fetuses showed strong reactivity at E15.5. In the experimental fetuses fibronectin was revealed the mesenchyma and basal lamina at E15.5. Taken together, it is suggested that maternal hyperthermia induces continuous expression of TGF-beta2 and FGF-8 in the mesenchyme and delayed expression of fibronectin. These should affect the normal palatogenesis and result in cleft palate.

The significance of PCD and mRNA transcription of p 53 gene during development of normal palate and cleft palate in C57BL/6N mouse / 实用口腔医学杂志

砄bjectives:To observe the difference of programmed cell death (PCD) and the expression of related gene p 53 in the development of normal palate and in the formation of cleft palate.Methods:The model of the development of cleft palat was estabished with retinoid acid (80 mg?kg 1 for each pregnant mouse). The palate samples were obtained at GD13 14 (at 13rd day 14 hours of prenancy),13 22 ,14 8,14 14 ,14 33 ,15 8,15 22 and 16 8 respectively.PCD was detected with TUNEL staining,while the mRNA transcription of p 53 was observed by in situ hybridization.Rssults:In early development of palate process,the positive index of PCD in the cleft palate samples was significantly higher than that in the normal ( P 0.05) between the two groups.Conclusion:The proliferation of mesenchymal cells of the early developmental palate process may be inhibited due to the abnomal PCD in the formation of cleft palate.The mechanism of PCD in this study may be a p 53 independed pathway.