Issue release date: 12.11.2024
2Celal Bayar University, Faculty of Medicine, Department of Histology-Embryology, Manisa, Turkey
3Celal Bayar University, Vocational School of Health Services, Manisa, Turkey
4Tepecik Women Health Care Hospital, Department of Pathology, Izmir, Turkey DOI : 10.5137/1019-5149.JTN.9428-13.0 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.
Keywords : Human fetus, Neural tube defect, TGF-βs, Smads