Study on etiology of retinoic acid-induced cleft palate in mouse.
- Author:
Hong-zhang HUANG
1
;
Bao-hui LÜ
;
Yi-yang CHEN
;
Gui-qing LIAO
Author Information
- Publication Type:Journal Article
- MeSH: Abnormalities, Drug-Induced; etiology; Animals; Cleft Palate; chemically induced; embryology; Embryo, Mammalian; Epidermal Growth Factor; biosynthesis; Female; Mice; Mice, Inbred C57BL; Palate; embryology; metabolism; Transforming Growth Factor beta; biosynthesis; Tretinoin; toxicity
- From: Chinese Journal of Stomatology 2003;38(3):185-187
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the morphologic changes of embryonic palatal development exposed to retinoic acid (RA) in mouse, and to detect the significance of the expression of TGFbeta1, TGFbeta3, EGF and BCL2.
METHODSThe stage of palatal development was examined by light microscopy. S-P immunohistochemistry and in-situ hybridization was used to detect spatio-temporal patterns of expression of TGFbeta1, TGFbeta3, EGF and BCL2 in embryonic palate.
RESULTSThe fetus exposed to RA resulted in formation of small palatal shelves without contact and fusion of each other to form and intact palate. RA can regulate the embryonic palatal expression of genes involved in RA-induced cleft palate.
CONCLUSIONSRA can inhibit the proliferation of MEPM cell to form small palatal shelves and induce abnormal differentiation of MEE cell causing the bi-palatal shelves no contact and fuse with each other, then induce the formation of cleft palate. RA can regulate the spatio-temporal patterns of expression of TGFbeta1, TGFbeta3 and EGF in embryonic palatal processes and the change of special expression of these genes in embryonic palatal processes are involved in RA-induced cleft palate.