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J Dent Res. 2011 Aug;90(8):981-7. doi: 10.1177/0022034511408613. Epub 2011 May 18.

Tgf-beta-mediated FasL-Fas-Caspase pathway is crucial during palatogenesis.

Author information

1
Department of Stomatology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China.

Abstract

Programmed cell death, or apoptosis, is one of the fates of the medial edge epithelium (MEE) during palatal fusion. Transforming growth factor β (Tgf-β) signaling (such as Tgf-β3) is required for the disappearance of the MEE, but the relationship between Tgf-β3 and apoptosis remains unclear. Here we show that the Fas ligand (FasL)-Fas-Caspase extrinsic apoptosis pathway functions during palatal fusion in wild-type mice, but is not detectable in mice lacking Tgf-β3 (Tgf-β3 (-/-) ) or Tgfβr2 in the MEE (K14-Cre;Tgfbr2 (fl/fl)). Inhibition of the FasL-Fas system results in persistence of the midline epithelial seam (MES) and inhibition of caspase activity during palatal organ culture. Moreover, ectopic FasL protein induces apoptosis in MES of K14-Cre;Tgfbr2 (fl/fl) mice. Thus, we conclude that the FasL-Fas-caspase extrinsic apoptosis pathway is regulated by the Tgf-β3 signaling cascade and is essential for palatal fusion during craniofacial development.

PMID:
21593251
PMCID:
PMC3170164
DOI:
10.1177/0022034511408613
[Indexed for MEDLINE]
Free PMC Article
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