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Int J Dev Biol. 1998 Sep;42(6):817-20.

Immunohistochemical localization of TGF-beta type II receptor and TGF-beta3 during palatogenesis in vivo and in vitro.

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1
The University of Southern California, School of Dentistry, Center for Craniofacial Molecular Biology, Los Angeles 90033, USA.

Abstract

The disappearance of medial edge epithelium (MEE) is a critical event for palate fusion. TGF-beta3 is one factor participating in the regulation of this process. To investigate the nature of ligand-receptor interactions in vivo between TGF-beta3 and the type II TGF-beta receptor (TbetaR-II), we compared the expression pattern of the receptor with TGF-beta3. Immunohistochemical analysis of the mouse fetus from E12 to E15 showed that expression of TbetaR-II in the palate began at E13 when the palatal shelves were in a vertical orientation. TbetaR-II was localized in the epithelial cells. This epithelium-favored distribution remained during palatal shelf elevation, the medial edge epithelial adherence, and midline epithelial seam disruption. After palate fusion and mesenchyme confluence, weak expression of TbetaR-II was present in the mesenchyme. To verify the possibility that TGF-beta3 and TbetaR-II expression coincide, immunohistochemistry was used to localize them both in serial sections. The distribution pattern of TGF-beta3 was also epithelium-limited in the palate from E13 to E15, and the spatial localization was correlated with the expression of TbetaR-II. Immunohistochemical localization of TbetaR-II and TGF-beta3 in palatal shelves in organ culture had patterns that were consistent with the in vivo results. These results suggest that TGF-beta3 exerts its developmental role through TbetaR-II in an autocrine fashion. The expression of both TGF-beta3 and TbetaR-II was below the detectable level in the mesenchyme following MEE disruption, suggesting that the TGF-beta3 signal might not be required once the MEE has completed phenotypic transformation/migration.

PMID:
9727838
[Indexed for MEDLINE]
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