TGF-βs and SMADs Activities at the Site of Failed Neural Tube in the Human Embryos
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AIM: Transforming growth factor beta (TGF-beta) and Smads control intracellular signaling pathways in neurulation. Although previously reported similar experimental animal studies, the aim of this human study is to investigate the expression of TGF-beta (1,2,3) and Smads (1,2,3,6,7) in aborted human fetuses with myeloschisis. MATERIAL and METHODS: Twelve human fetuses with neural tube defect were obtained. They were stained with antibodies against TGF-beta 1, TGF-beta 2,TGF-beta 3, Smad (1,2,3), Smad 6 and Smad 7 using the indirect immunohistochemical technique. RESULTS: We noted mild immune reactivity of TGF-beta 1 and TGF-beta 2 in the open neural plate, motor neurons and surrounding tissue. Strong immune reactivity of TGF-beta 3 was shown in only open neural plate and surrounding tissue. Immunoreactivity of all Smads noted negative except Smad7. CONCLUSION: These results suggested at the site where the neural tube failed to close, TGF-beta 1,2 and Smads 1,2,3,6 do not continue their activity and decrease with internal timing of embryonic development. Additionally ectodermal layers are considered by embryo asnot closed wound and TGF-beta 3 activity may be an effort to repair the failed closure.