4.4 Article

Perturbation of Fgf10 signal pathway in mouse embryonic palate by dexamethasone and vitamin B12 in vivo

Journal

JOURNAL OF PEDIATRIC SURGERY
Volume 45, Issue 10, Pages 2030-2035

Publisher

W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.jpedsurg.2010.05.018

Keywords

Cleft palate; Dexamethasone; Vitamin B; Proliferation; Fgf10; Fgfr2b; Shh

Funding

  1. National Natural Science Foundation of China [30530730]

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Background/Purpose: The Fgf10 signaling pathway plays an important role in early stages of mouse embryonic palatal development, which is associated with cell proliferation and differentiation. The objective of this study was to assess whether dexamethasone and vitamin B-12 affected the Fgf10 signal pathway of mouse embryonic palate. Materials and Methods: Immunohistochemical studies were performed for expression of Fgf10, Fgfr2b, and sonic hedgehog and for cell proliferation and apoptosis of mouse embryonic palate. Results: The expression of Fgf10, Fgfr2b, and sonic hedgehog was changed inmouse embryonic palate after dexamethasone and vitamin B-12 treatment, resulting in reduced and restored proliferation of mesenchymal cells. Conclusions: Dexamethasone and vitamin B-12 affected the Fgf10 signaling pathway and cell proliferation of mouse embryonic palate. Cell apoptosis was not altered after dexamethasone and vitamin B-12 exposure. (C) 2010 Published by Elsevier Inc.

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