| First Author | Huang X | Year | 2011 |
| Journal | J Dent Res | Volume | 90 |
| Issue | 8 | Pages | 981-7 |
| PubMed ID | 21593251 | Mgi Jnum | J:196045 |
| Mgi Id | MGI:5486436 | Doi | 10.1177/0022034511408613 |
| Citation | Huang X, et al. (2011) Tgf-beta-mediated FasL-Fas-Caspase pathway is crucial during palatogenesis. J Dent Res 90(8):981-7 |
| abstractText | Programmed cell death, or apoptosis, is one of the fates of the medial edge epithelium (MEE) during palatal fusion. Transforming growth factor beta (Tgf-beta) signaling (such as Tgf-beta3) is required for the disappearance of the MEE, but the relationship between Tgf-beta3 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-beta3 (Tgf-beta3 (-/-) ) or Tgfbetar2 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-beta3 signaling cascade and is essential for palatal fusion during craniofacial development. |
