Barutcuoglu M.Umur A.S.Vatansever H.S.Umur N.Ozbilgin K.Sayhan S.Selcuki M.2024-07-222024-07-22201310195149http://akademikarsiv.cbu.edu.tr:4000/handle/123456789/17432Aim: Transforming growth factor β (TGF-β) 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-β (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-β1, TGF-β2, TGF-β3, Smad (1,2,3), Smad 6 and Smad 7 using the indirect immunohistochemical technique. Results: We noted mild immune reactivity of TGF-β1 and TGF-β2 in the open neural plate, motor neurons and surrounding tissue. Strong immune reactivity of TGF-β3 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-β 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-β3 activity may be an effort to repair the failed closure.EnglishAdultColoring AgentsFemaleHumansImmunohistochemistryMaleNeural TubeNeural Tube DefectsParaffin EmbeddingPregnancySignal TransductionSmad ProteinsTissue FixationTransforming Growth Factor betacoloring agentparaffinSmad proteintransforming growth factor betaadultarticlefemalehumanimmunohistochemistrymalemetabolismneural tubeneural tube defectpathologypregnancyprenatal developmentsignal transductiontissue fixationTGF-βs and SMADs activities at the site of failed neural tube in the human embryosArticle10.5137/1019-5149.JTN.9428-13.0