Journals / Turkish Neurosurgery / 2016 / Cilt: 26 - Sayı: 4

Targeting Apoptosis Through FOXP1, and N-cadherin with Glatiramer Acetate in Chick Embryos During Neural Tube Development

Pages
586–594
DOI
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CONCLUSION: GA affects the spinal cord development through FOXP in the chick embryo model at high doses.

📌 3 Key Takeaways

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Objective & Hypothesis: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.
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Key Findings & Data:MATERIAL and METHODS: One hundred fertile, specific pathogen free eggs were divided into 5 groups for this study.
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Conclusion & Impact:CONCLUSION: GA affects the spinal cord development through FOXP in the chick embryo model at high doses.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

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 ?l physiological saline; in Group 2 the embryos (n=20) were given 10 ?l GA (equal to daily human therapeutic dose); 20 ?l GA (equal to twice daily human therapeutic dose) was injected to embryos in Group 3 (n=20); in Group 4 and 5, 30 ?l and 40 ?l 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.

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Cite This Article

TAŞKAPILIOĞLU, M. Ö., BİLLUR, D., KIZIL, Ş., TAŞKAPILIOĞLU, Ö., OCAKOĞLU, G., AYDIN, S., BEKAR, A., ÜNLÜ, A. (2016). Targeting Apoptosis Through FOXP1, and N-cadherin with Glatiramer Acetate in Chick Embryos During Neural Tube Development. Turkish Neurosurgery, Cilt: 26 - Sayı: 4, 586–594. https://ajindex.com/articles/404717

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References (3)

  1. Arnon R: The development of Cop 1 (Copaxone), an innovative drug for the treatment of multiple sclerosis: Personal reflections. Immunol Lett 50:1-15, 1996 2. Arnon R, Aharoni R: Mechanism of action of glatiramer acetate in multiple sclerosis and its potential for the development of new applications. Proc Natl Acad Sci U S A 101:14593-14598, 2004 3. Banham AH, Beasley N, Campo E, Fernandez PL, Fidler C, Gatter K, Jones M, Mason DY, Prime JE, Trougouboff P, Wood K, Cordell JL: The FOXP1 winged helix transcription factor is a novel candidate tumor suppressor gene on chromosome 3p. Cancer Res 61: 8820-8829, 2001 4. Banham AH, Connors JM, Brown PJ, Cordell JL, Ott G, Sreenivasan G, Farinha P, Horsman DE, Gascoyne RD: Expression of the FOXP1 transcription factor is strongly associated with inferior survival in patients with diffuse large B-cell lymphoma. Clin Cancer Res 11: 1065-1072, 2005 5. Barrans SL, Fenton JA, Banham A, Owen RG, Jack AS: Strong expression of FOXP1 identifies a distinct subset of diffuse large B-cell lymphoma (DLBCL) patients with poor outcome. Blood 104: 2933-2935, 2004 6. Carlsson P, Mahlapuu M: Forkhead transcription factors: Key players in development and metabolism. Dev Biol 250:1-23, 2002 7. Carpintero R, Brandt KJ, Gruaz L, Molnarfi N, Lalive PH, Burger D: Glatiramer acetate triggers PI3Kdelta/Akt and MEK/ ERK pathways to induce IL-1 receptor antagonist in human monocytes. Proc Natl Acad Sci U S A 107:17692-17697, 2010 8. Cecconi F, Piacentini M, Fimia GM: The involvement of cell death and survival in neural tube defects: A distinct role for apoptosis and autophagy? Cell Death Differ 15:1170-1177, 2008 9. Chatila TA, Blaeser F, Ho N, Lederman HM, Voulgaropoulos C, Helms C, Bowcock AM: JM2, encoding a fork headrelated protein, is mutated in X-linked autoimmunity-allergic disregulation syndrome. J Clin Invest 106:75-81, 2000 10. Cohen JA, Rovaris M, Goodman AD, Ladkani D, Wynn D, Filippi M
  2. 9006 Study Group: Randomized, double-blind, dose-comparison study of glatiramer acetate in relapsingremitting MS. Neurology 68: 939-944, 2007 11. Comi G, Cohen JA, Arnold DL, Wynn D, Filippi M
  3. FORTE Study Group: Phase III dose-comparison study of glatiramer acetate for multiple sclerosis. Ann Neurol 69: 75-82, 2011 12. Copp AJ, Brook FA, Estibeiro JP, Shum AS, Cockroft DL: The embryonic development of mammalian neural tube defects. Prog Neurobiol 35: 363-403, 1990 13. Cragan JD, Roberts HE, Edmonds LD, Khoury MJ, Kirby RS, Shaw GM, Velie EM, Merz