TGF-βs and SMADs activities at the site of failed neural tube in the human embryos

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dc.contributor.authorBarutcuoglu M.
dc.contributor.authorUmur A.S.
dc.contributor.authorVatansever H.S.
dc.contributor.authorUmur N.
dc.contributor.authorOzbilgin K.
dc.contributor.authorSayhan S.
dc.contributor.authorSelcuki M.
dc.date.accessioned2025-04-10T11:14:23Z
dc.date.available2025-04-10T11:14:23Z
dc.date.issued2013
dc.description.abstractAim: 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.
dc.identifier.DOI-ID10.5137/1019-5149.JTN.9428-13.0
dc.identifier.urihttp://hdl.handle.net/20.500.14701/50254
dc.publisherTurkish Neurosurgical Society
dc.titleTGF-βs and SMADs activities at the site of failed neural tube in the human embryos
dc.typeArticle

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