The corneal epithelium is a self-renewing tissue and must, by definition, have a resident basal cell population necessary for homeostasis and wound healing. There is a substantial body of evidence, both experimental and clinical, pointing to the basal cells of the limbus as the location of corneal epithelial stem cells. However, in the absence of a definitive marker of limbal stem cells, the evidence remains largely circumstantial. Many markers such as p63 and integrin alpha9 are preferentially localized to the limbus but cannot be regarded as stem cell-specific. Other markers such as K3 and connexin 43 can be regarded as markers of corneal differentiation. The discovery of stem cell markers in other organ systems, such as the haematopoietic system, offers optimism that a marker of limbal stem cells will one day be found. Such a discovery will have far-reaching implications for the study of ocular surface biology and stratified squamous epithelia in general.

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A wide variety of retinal pathology is associated with an increase in Müller glial cell expression of glial fibrillary acidic protein (GFAP). In this study the time course and spatial spread of the Müller cell GFAP response following argon laser photocoagulation lesions was examined in wholemounted rabbit retina. At 24 hours single focal lesions were surrounded by GFAP positive Müller cell end feet which declined in density with distance but extended as far as 2-3 mm from the lesion. The Müller cell reaction reached a maximal spread of 4-5 mm at 14 to 21 days and had started to contract by 30 days, leaving a core of GFAP positive processes immediately around the lesion site at 60 days. This zone of spread was much larger than the area of disrupted pigment epithelium. Isodensity plots did not reveal any correlation with the trajectory of retinal ganglion cell axons. The spread of reaction was more confined for lesions within the visual streak than in the dorsal or ventral retinal periphery. Multiple lesions within a focal region of retina resulted in a greater density of GFAP reactive end feet with a corresponding greater spread. However, when five to ten lesions were made in a horizontal row, the Müller cells over the entire retina became GFAP immunoreactive. This pan-retinal reaction took several days to spread, peaked at 7-14 days, and contracted back to the primary lesion sites by 2 months. This spread of Müller cell reactivity may be triggered by the diffusion of substances released by injury or it may be due to direct cellular communication. The extensive indirect effect on Müller cells of laser irradiation might be an important component of the clinical effect of laser photocoagulation and indicates a long distance communication mechanism between retinal glia which is poorly understood. This study also shows the importance of the time at which the Müller cell response is assessed.