Retinal pigment cells were dislodged from normal monkey eyes and incubated in glass-slide chambers. All viable pigment cells adhered strongly to glass. They demonstrated surface receptors for the Fc portion of immunoglobulin G and for the third component of complement by selectively binding and phagocytizing antibody or complement-coated erythrocytes. These phagocytic cells with receptors were identified as retinal pigment cells by characteristic ultrastructural features. Thus, retinal pigment cells, which are generally believed to be derived from neural tissue, are not only scavengers of photoreceptor cell debris, but also have surface receptors and phagocytic functions that may be important in ocular defense.
To assess the extent to which endothellal cell (EC) structure Is modified by hyperllpldemla and by the formation of Irrtlmal plaques, we undertook a quantitative ultrastructural study of aortic EC of cynomolgus monkeys after 3 or 6 months on an atherogenic diet We compared EC In lesion-free areas ( I n an earlier study of diet-induced atherogenesis in the cynomolgus monkey, 1 we reported that endothelial cells were markedly attenuated over early intimaJ foam cell accumulations, but we could find no evidence of endothelial cell (EC) degeneration, disruption, or desquamation either over lesions or in lesion-free areas. Interruptions of lumen surface continuity occurred only over Received September 20, 1988; revision accepted June 27, 1989. some multilayered confluent lesions where foam cells penetrated between adjacent endothelial cells or through pores or gaps in endothelial cell bodies. Subsequent investigations in rabbits and in stump-tail monkeys 2 -3 also revealed that diet-induced lesions were not associated initially with EC disruption. Platelet deposition over more advanced plaques has been considered a consequence of endotheliaJ discontinuities, which develop with continued plaque deposition. It has been proposed 4 that such changes are a basis for the transition from fatty streaks to complex plaques. Whether or not EC disruption actually occurs as a complication of plaque enlargement, the attenuation and reshaping of EC over earty intimal lesions suggests a plasticity that would tend to preserve the integrity of the endotheliaJ lining.In an attempt to characterize this presumably adaptive process, we undertook a quantitative investigation of EC
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