التفاصيل البيبلوغرافية
| العنوان: |
MFGE8 Does Not Influence Chorio-Retinal Homeostasis or Choroidal Neovascularization in vivo. |
| المؤلفون: |
Raoul, William1,2,3 william.raoul@inserm.fr, Poupel, Lucie4,5, Tregouet, David-Alexandre6,7, Lavalette, Sophie1,2,3, Camelo, Serge6,8,9, Keller, Nicole6,8,9, Krumeich, Sophie10,11, Calippe, Bertrand1,2,3, Guillonneau, Xavier1,2,3, Behar-Cohen, Francine6,8,9,12, Cohen, Salomon-Yves13, Baatz, Holger14, Christophe Combadière4,5,15, Théry, Clotilde10,11, Sennlaub, Florian1,2,3,12 florian.sennlaub@inserm.fr |
| المصدر: |
PLoS ONE. Mar2012, Vol. 7 Issue 3, p1-8. 8p. |
| مصطلحات موضوعية: |
*MILKFAT, *EPIDERMAL growth factor, *PHAGOCYTOSIS, *SINGLE nucleotide polymorphisms, *SCANNING electron microscopy, *NEOVASCULARIZATION, *GALACTOSIDASES |
| مستخلص: |
Purpose: Milk fat globule-epidermal growth factor-factor VIII (MFGE8) is necessary for diurnal outer segment phagocytosis and promotes VEGF-dependent neovascularization. The prevalence of two single nucleotide polymorphisms (SNP) in MFGE8 was studied in two exsudative or ''wet'' Age-related Macular Degeneration (AMD) groups and two corresponding control groups. We studied the effect of MFGE8 deficiency on retinal homeostasis with age and on choroidal neovascularization (CNV) in mice. Methods: The distribution of the SNP (rs4945 and rs1878326) of MFGE8 was analyzed in two groups of patients with ''wet'' AMD and their age-matched controls from Germany and France. MFGE8-expressing cells were identified in Mfge8+/- mice expressing ß-galactosidase. Aged Mfge8+/- and Mfge8-/- mice were studied by funduscopy, histology, electron microscopy, scanning electron microscopy of vascular corrosion casts of the choroid, and after laser-induced CNV. Results: rs1878326 was associated with AMD in the French and German group. The Mfge8 promoter is highly active in photoreceptors but not in retinal pigment epithelium cells. Mfge8-/- mice did not differ from controls in terms of fundus appearance, photoreceptor cell layers, choroidal architecture or laser-induced CNV. In contrast, the Bruch's membrane (BM) was slightly but significantly thicker in Mfge82/2 mice as compared to controls. Conclusions: Despite a reproducible minor increase of rs1878326 in AMD patients and a very modest increase in BM in Mfge8-/- mice, our data suggests that MFGE8 dysfunction does not play a critical role in the pathogenesis of AMD. [ABSTRACT FROM AUTHOR] |
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