Pericyte response during choriocapillaris atrophy in the rabbit.
The rabbit and rat choriocapillaris atrophies in response to experimental destruction of the retinal pigment epithelium by intravenous injection of sodium iodate. This provides a convenient model of capillary atrophy. We have observed that pericytes are spared during this process; the atrophy is due to loss of endothelium only. Extensive examination of thin sections obtained 1 day to 11 weeks after administration of iodate showed that pericytes retained their normal relationship to the remnant capillary basement membrane left behind as the endothelial tube atrophied. This was most conspicuously manifested in their retention of processes longitudinally disposed along the sleeves of remnant basement membrane. The processes retained bundles of actin filaments that had dense regions along them and inserted into subplasmalemmal densities at basement membrane attachment sites, i.e. they had the characteristics of stress fibers. The pericytes did not phagocytose the debris of endothelial necrosis, in spite of their known phagocytic abilities. Necrotic endothelial cells were eliminated by sloughing into the capillary lumen. The observations support the idea that the function of pericytes in the choriocapillaris, the major source of nutrition for the retinal photoreceptors, resides in their contractility, and that pericytes do not remove necrotic endothelium during capillary atrophy.
Korte
G E
GE
Department of Ophthalmology, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, N.Y.
Pua
F
F
D000199:Actins / Q000032:analysis; D000818:Animals; D001158:Arteries / Q000503:physiopathology*; D001160:Arterioles / Q000032:analysis / Q000473:pathology / Q000503:physiopathology* / Q000648:ultrastructure; D001284:Atrophy / Q000139:chemically induced / Q000473:pathology; D001485:Basement Membrane / Q000503:physiopathology / Q000648:ultrastructure; D002196:Capillaries / Q000473:pathology* / Q000503:physiopathology; D002829:Choroid / Q000098:blood supply / Q000473:pathology*; D004195:Disease Models, Animal / Q000139:chemically induced / Q000473:pathology; D004730:Endothelium, Vascular / Q000503:physiopathology / Q000648:ultrastructure; D007452:Iodates / Q000494:pharmacology; D011817:Rabbits
D000199:Actins; D007452:Iodates; C032285:sodium iodate