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Gsk3β in palatal development
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.984.4
Subject(s) - gsk 3 , wnt signaling pathway , pi3k/akt/mtor pathway , glycogen synthase , phosphorylation , signal transduction , biology , blot , microbiology and biotechnology , chemistry , biochemistry , gene
Background: Glycogen synthase kinase‐3β (Gsk‐3β) has multiple roles in development and disease. Gsk3β homozygous null mice have a complete cleft palate and can be rescued by restoring the endogenous Gsk‐3β activity. Gsk‐3β has regulatory roles in Wnt, PI3‐Kinase(PI3K), ILK and insulin signaling pathways. In order to investigate the specific signal that regulates the Gsk3β activity, we examined two potential upstream factors: PI3K and Wnt3a during palatal development. Materials and methods: E13.5 embryos were dissected from the pregnant females (CD1). The palatal shelves were placed in organ culture on filter paper with the nasal surface facing down. Tissues were cultured in BGJ b medium for 24hrs. PI3K inhibitor, LY294002 (1μM and 10μM) was added to some groups. Tissues were analyzed with western blots and immunofluorescent staining. Results: GSK3β and p‐Gsk3β (phosphorylated Gsk3β) were both expressed in palatal tissue at E13.5 and after 24hr culture. Previously, Wnt3a was reported to crosstalk with TGFβ signals to regulate palatal growth, but we did not detect Wnt3a protein. The PI3K inhibitor, did not change Gsk3β and p‐Gsk3β at the dose and time studied. Conclusion: Although PI3K was necessary for palatal fusion; Gsk3β does not change phosphorylation state in PI3K inhibitor treated palatal shelves in the first 24hr. This work is supported by March of Dimes Research grant (FY06‐321)