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A TGF-beta-induced gene, betaig-h3, is crucial for the apoptotic disappearance of the medial edge epithelium in palate fusion.
Cited 12 time in
Web of Science
Cited 12 time in Scopus
- Authors
- Issue Date
- 2009-03
- Publisher
- Wiley-Blackwell
- Citation
- Journal of Cellular Biochemistry 107:818–825
- Keywords
- TGF-b3 ; big-h3 ; MEDIAL EDGE EPITHELIUM (MEE) ; APOPTOSIS ; PALATE ; CLEFT ; ANTISENSE ; RGD
- Abstract
- TGF-b3, TbR-I, and TGF-b-activated Smad2 has been suggested to be a series of signaling molecules for secondary palate fusion. In this
article, we show that a gene induced by TGF-b, big-h3, is coincidentally expressed with TGF-b3 in medial edge epithelial (MEE) cells
undergoing apoptosis during normal palatal fusion. big-h3 was also highly expressed in the areas of post-weaning mammary gland cells and
developing phalangeal joints in which TGF-b3 or BMP-4-induced apoptosis occurs, respectively. Blocking of big-h3 expression in E12.5
embryos with antisense oligodeoxynucleotides (ODN) resulted in cleft of the secondary palate in 84% of the treated mice that were born.
Moreover, the antisense ODN treatment resulted in a failure of apoptosis in the MEE between palatal shelves in physical contact in organ
culture. We conclude that big-h3 expression in the MEE is stimulated by TGF-b3, causes cell death, and consequently results in complete
fusion of the apposed palatal shelves.
- ISSN
- 0730-2312
- Language
- English
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