Sb. Smith et al., REDUCTION OF PHAGOSOMES IN THE VITILIGO (C57BL 6-MI(VIT)/MI(VIT)) MOUSE MODEL OF RETINAL DEGENERATION/, Investigative ophthalmology & visual science, 35(10), 1994, pp. 3625-3632
Purpose. The vitiligo (C57BL/6-mi(vit)/mi(vit)) mouse has a slowly pro
gressing retinal degeneration, in which photoreceptor cell nuclei are
gradually lost and the retinal pigment epithelium (RPE) is unevenly pi
gmented. The purpose of the present study was to assess the phagocytic
ability of the RPE in the vitiligo mouse by determining whether and w
hen a phagocytic burst occurs in affected mice and whether the number
of phagosomes varies between control and affected animals. Methods. Ey
es of control and vitiligo mice 4 to 20 weeks of age were embedded in
Spurr. Thin sections were cut and examined by electron microscopy to c
onfirm the presence of phagosomes, particularly in the affected animal
s. Thick (1 mu m) sections were cut, and quantitative morphometry was
performed at the light microscope level. The length of RPE was determi
ned, and phagosomes were counted in RPE cytoplasmic and microvillous a
reas. Data were expressed as phagosomes per 1000 mu m. Results. The vi
tiligo mouse has a peak phagocytic episode approximately 2 hours after
light onset. The number of phagosomes in 4-week-old affected mice was
significantly less than that in controls (13 phagosomes per 1000 mu m
compared to 30 phagosomes per 1000 mu m). By week 8, the number was r
educed to approximately 5 per 1000 mu m. Phagosome number was not redu
ced further between weeks 8 and 20 in the affected animal. Macrophage-
like cells containing pigment granules and phagosomes were observed in
the subretinal space in areas where the rod outer segments had been s
eparated from the RPE. Conclusions. The vitiligo mouse RPE contains ph
agosomes, but there are significantly fewer than in controls. It is no
t known whether a defect in RPE phagocytosis is the direct cause of th
e retinal defect in this model.