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A TGF‐β‐induced gene, βig‐h3, is crucial for the apoptotic disappearance of the medial edge epithelium in palate fusion
Author(s) -
Choi KangYoung,
Kim HyunJung,
Cho ByungChae,
Kim InSan,
Kim HyunJung,
Ryoo HyunMo
Publication year - 2009
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22180
Subject(s) - apoptosis , microbiology and biotechnology , epithelium , fusion gene , transforming growth factor , biology , gene , genetics
Abstract TGF‐β3, TβR‐I, and TGF‐β‐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‐β, βig‐h3, is coincidentally expressed with TGF‐β3 in medial edge epithelial (MEE) cells undergoing apoptosis during normal palatal fusion. βig‐h3 was also highly expressed in the areas of post‐weaning mammary gland cells and developing phalangeal joints in which TGF‐β3 or BMP‐4‐induced apoptosis occurs, respectively. Blocking of βig‐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 βig‐h3 expression in the MEE is stimulated by TGF‐β3, causes cell death, and consequently results in complete fusion of the apposed palatal shelves. J. Cell. Biochem. 107: 818–825, 2009. © 2009 Wiley‐Liss, Inc.