A TGF-β-induced gene, βig-h3, is crucial for the apoptotic disappearance of the medial edge epithelium in palate fusion

Kang Young Choi, Hyun Jung Kim, Byung Chae Cho, In San Kim, Hyun Jung Kim, Hyun Mo Ryoo

Research output: Contribution to journalArticle

11 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)818-825
Number of pages8
JournalJournal of cellular biochemistry
Volume107
Issue number4
DOIs
Publication statusPublished - 2009 Jul 1
Externally publishedYes

Keywords

  • Antisense
  • Apoptosis
  • Cleft
  • Medial edge epithelium (MEE)
  • Palate
  • RGD
  • TGF-β3; βig-h3

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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