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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  Mfge8 −/−   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.

MFGE8 Does Not Influence Chorio-Retinal Homeostasis or Choroidal Neovascularization in vivo