Targeting Apoptosis Through Foxp1, and N-cadherin with Glatiramer Acetate in Chick Embryos During Neural Tube Development
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Published on: May 11, 2019
M Ozgur Taskapilioglu1, Deniz Billur, Sule Kizil
1Uludag University, Faculty of Medicine, Department of Neurosurgery, Bursa, Turkey.
Aim:
To demonstrate the effect of glatiramer acetate (GA) in chick embryos on neural tube (NT) development, and to explore its effects of Foxp1, apoptosis, and N-cadherin.
Material And Methods:
One hundred fertile, specific pathogen free eggs were divided into 5 groups for this study. The eggshell was windowed specifically at 24 hours of incubation. The embryos in Group 1 (n=20) were treated with 10 μl physiological saline; in Group 2 the embryos (n=20) were given 10 μl GA (equal to daily human therapeutic dose); 20 μl GA (equal to twice daily human therapeutic dose) was injected to embryos in Group 3 (n=20); in Group 4 and 5, 30 μl and 40 μl GA were administered to the embryos (n=20) (equal to x3 and x4 daily human therapeutic dose, respectively). Each egg was re-incubated for 24 hours more. Then, histological and immunohistochemical evaluation of the subjects were done.
Results:
The embryos with NT defect showed FOXP1 expression without N- cadherin or staining with N-cadherin in another location in our study. We interpreted this result as GA leading to an NT closure defect by increasing FOXP expression. Moreover, we also showed the reverse relation between FOXP1 and N-cadherin at the immunohistochemical level for the first time.
Conclusion:
GA affects the spinal cord development through FOXP in the chick embryo model at high doses.
Insights
High doses of glatiramer acetate (GA) disrupt neural tube development in chick embryos by increasing FOXP1 expression, affecting spinal cord formation. This study reveals a novel inverse relationship between FOXP1 and N-cadherin during this process.
Area of Science:
- Developmental biology
- Neuroscience
- Immunology
Background:
- Glatiramer acetate (GA) is used to treat multiple sclerosis.
- Neural tube (NT) defects can arise from complex molecular interactions during embryonic development.
Purpose of the Study:
- To investigate the impact of glatiramer acetate (GA) on chick embryo neural tube (NT) development.
- To explore the effects of GA on Foxp1 expression, apoptosis, and N-cadherin.
Main Methods:
- Fertile chick embryos were divided into five groups and treated with varying doses of GA or saline.
- Histological and immunohistochemical analyses were performed after 24 hours of incubation.
Main Results:
- GA administration, particularly at higher doses, was associated with neural tube defects.
- Increased FOXP1 expression was observed in embryos with NT defects.
- A novel inverse relationship between FOXP1 and N-cadherin expression was identified.
Conclusions:
- Glatiramer acetate (GA) can adversely affect spinal cord development in chick embryos at elevated concentrations.
- FOXP1 plays a significant role in GA-induced neural tube defects.
