NORMALLY OCCURRING LOSS OF SINGLE CELLS AND REPAIR OF RESULTING DEFECTS IN RETINAL-PIGMENT EPITHELIUM IN-SITU

The retinal pigment epithelial cells, which form a monolayer between t he choroid and photoreceptor cell layer of the eye, generally do not d ivide after birth. There is, however, a gradual loss of retinal pigmen t epithelial cells with increasing age and an increase in the size of those remaining. How retinal pigment epithelial cells die and the mech anism by which the integrity of retinal pigment epithelium is maintain ed after cell death has not been examined. Confocal laser scanning mic roscopy of whole mounts of retinal pigment epithelium of 12 to 16 day old chick embryos showed that among the great majority of retinal pigm ent epithelial cells which were regular in size and hexagonal in shape , single, scattered, irregularly shaped, dying cells are present. The distribution of the dying retinal pigment epithelial cells, their morp hology and the presence of apoptotic bodies, including pyknotic and fr agmented nuclei, above such defects suggests that the death occurs by apoptosis. The defects created by the dying or dead cells were repaire d by spreading of the surrounding normal retinal pigment epithelial ce lls and a series of stages in the repair of the defects could be ident ified. During the repair of the defects, fine microfilament bundles ru nning parallel to the edge of the defect in each of the surrounding re tinal pigment epithelial cells could be detected by confocal laser sca nning microscopy giving a 'spider-web' appearance to the region around the defect. Since induction of proliferation in retinal pigment epith elial cells during healing of the defect requires cell migration, rye would not expect the spreading of retinal pigment epithelial cells int o the single cell defects to trigger cell proliferation. The death of single cells and the spreading of adjacent ones in the absence of cell proliferation would however explain at least in part the increase in the average size of retinal pigment epithelial cells with age. (C) 199 6 Academic Press Limited