TGF-ßs and Smads activities at the site of failed neural tube in the human embryos.

ABSTRACT

AIM: Transforming growth factor ß (TGF-ß) 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-ß (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-ß1, TGF-ß2, TGF-ß3, Smad (1,2,3), Smad 6 and Smad 7 using the indirect immunohistochemical technique. RESULTS: We noted mild immune reactivity of TGF-ß1 and TGF-ß2 in the open neural plate, motor neurons and surrounding tissue. Strong immune reactivity of TGF-ß3 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-ß 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 as "not closed wound" and TGF-ß3 activity may be an effort to repair the failed closure.