TGF-βs and SMADs activities at the site of failed neural tube in the human embryos
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Date
2013
Authors
Barutcuoglu M.
Umur A.S.
Vatansever H.S.
Umur N.
Ozbilgin K.
Sayhan S.
Selcuki M.
Journal Title
Journal ISSN
Volume Title
Publisher
Turkish Neurosurgical Society
Abstract
Aim: 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.
Description
Keywords
Adult, Coloring Agents, Female, Humans, Immunohistochemistry, Male, Neural Tube, Neural Tube Defects, Paraffin Embedding, Pregnancy, Signal Transduction, Smad Proteins, Tissue Fixation, Transforming Growth Factor beta, coloring agent, paraffin, Smad protein, transforming growth factor beta, adult, article, female, human, immunohistochemistry, male, metabolism, neural tube, neural tube defect, pathology, pregnancy, prenatal development, signal transduction, tissue fixation