Nicotine inhibits palatal fusion and modulates nicotinic receptors and the PI3 kinase pathway in medial edge epithelia*
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Structured AbstractAuthors Kang P, Svoboda KKHObjectives To analyze the effects of nicotine on palatal fusion inhibition in vitro and determine if nicotine modulated transforming growth factor 3 or phosphatidylinositol3 kinase signaling. A second objective was to determine the localization and regulation of nicotinic receptors in the medial edge epithelia (MEE) during palatal fusion.Design Palatal shelves from embryonic day (E) 13.5 mice were cultured in serum free media and treated with 0, 0.06, 0.6, or 6mM nicotine, nicotinic receptor antagonist bungarotoxin, or the combination of nicotine and bungarotoxin. Tissues harvested at 72h were analyzed for epithelialmesenchymal transformation (EMT) and fusion. MEE samples collected at 20h were analyzed for phosphorylated AktSer473, phosphorylated Smad2, and nicotinic receptors.Results Nicotine inhibited palatal fusion in vitro in a dose dependent manner. Activated AktSer473 was greater in control MEE than in nicotine treated tissues; while there was no difference in activated Smad2 between groups. The 7 subunit of nicotinic receptor was expressed in MEE during palate fusion and increased in nicotine treated tissues. Alphabungarotoxin did not rescue the nicotine treated palates.Conclusion Nicotine treatment had no effect on Smad2, but caused a down regulation of the PI3 kinase pathway that may have contributed to inhibiting palatal fusion in vitro.
