Turkish Neurosurgery 2013 , Vol 23 , Num 6
TGF-βs and Smads Activities at the Site of Failed Neural Tube in the Human Embryos
Mustafa BARUTCUOGLU1, Ahmet Sukru UMUR1, Hatice Seda VATANSEVER2, Nurcan UMUR3, Kemal OZBILGIN2, Sevil SAYHAN4, Mehmet SELCUKI1
1Celal Bayar University, Faculty of Medicine, Department of Neurosurgery, Manisa, Turkey
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

Corresponding author : Mustafa Barutcuoglu, barutcum@yahoo.com