Research Paper Volume 5, Issue 6 pp 427—444

Deficiency in the metabolite receptor SUCNR1 (GPR91) leads to outer retinal lesions

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Figure 4. SUCNR1 deficient microglia show impaired migration and accumulate in the subretinal space. (A) Migration assays performed in modified Boyden chambers demonstrate that macrophages from Sucnr1−/− mice have compromised chemotaxis towards oxLDL. The migratory potential of macrophages was not enhanced by treatment with succinate (100μM) (n=7). *P<0,05. (B-C) RPE flatmounts extracted at 8 weeks reveal a significant (D) accumulation of microglia in Sucnr1−/− mice when compared to wild-type controls. **P<0,01. Upon receiving high fat diets, the number of sub-retinal microglia did not vary (G) but were bloated (E,F). *P<0,05. Phalloidin stain of RPE flatmounts shows that RPE morphology is intact at 8 weeks in both knockout and controls (H,I), and that microglia (IBA1:green) remain on the retinal side of RPE (J-L). At 20 weeks, microglia (IBA1;green) puncture (M-O) and penetrate the RPE (P,Q). A portion of microglia remain on the retinal side of the RPE at 20 weeks as determined by transmission electron microscopy (R). Scale bar (B,C,E,F): 50μm,(I): 50μm, (J-Q) 20μm, (R): 5μm.