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Inside IOVS 2001
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April 2001 |
Restoring Function in Ocular Disease
Natural Tear Substitutes for Dry Eye
Serum and saliva have been advocated as natural tear substitutes for intractable dry eyes, but their effects on corneal epithelium are not well characterized. A laboratory study by Geerling et al. (p. 948) used a fully defined test model of primary human corneal epithelial cells to compare the toxicity of these natural tear substitutes with pharmaceutical substitutes. Natural tear substitutes maintained microvillous density, cell membrane permeability, intracellular esterase activity and levels of ATP better than unpreserved pharmaceutical tear substitutes. Serum and isotonic, but not natural, saliva have better therapeutic potential for severely dry eyes than pharmaceutical tear substitutes.
BDNF Rescue in Glaucoma
Retinal ganglion cell (RGC) degeneration is an unfortunate result of many optic neuropathies. In glaucoma, pressure-induced disruption of the transport of target-derived trophic material has been suggested as one possible mechanism underlying ganglion cell death. Previous studies have demonstrated that brain-derived neurotrophic factor (BDNF) is highly effective in reducing axotomy-induced RGC death in the small rat eye. Chen and Weber (p. 966) show that BDNF also is an effective neuroprotectant in the cat eye, which is similar in size and neuronal cell type to the primate eye. This supports a potential therapeutic role for BDNF in the treatment of human glaucoma.
Anti-CD154 Therapy in Corneal Transplantation
Corneal transplantation provides the only hope for restoring sight for tens of thousands of corneally blind patients annually. However, many corneal grafts fail from immune rejection. Interaction between CD40 and CD154 represents a critical costimulatory pathway for immune activation. Qian et al. (p. 987) show near-universal acceptance of corneal grafts by systemic administration of anti-CD154 antibody which selectively prevents activation of interferon-gamma secreting T helper 1 cells that mediate transplant rejection. These findings support the feasibility of selective immunomodulatory strategy as a means of reducing corneal allograft rejection.
Restoration of Light Response after Retinal Transplantation
Functional integration of the graft and host retina has not been conclusively demonstrated following neural retinal transplantation in animal models of retinal degeneration. Host characteristics such as the age of the host may be important factors that affect the success of this procedure. Radner et al. (p. 1057) demonstrate the restoration of retinal ganglion cell responses to light following the transplantation of neural retinal tissue into the eyes of retinal degenerate (rd) mice at an age of only two weeks.
LEDGF Rescue in Retinal Degeneration
A novel growth factor, recently isolated from the lens, lens epithelium-derived growth factor (LEDGF) was shown to promote growth and survival of cultured lens epithelial and retinal cells. Machida et al. (p. 1087) show that a single injection of LEDGF produces substantial photoreceptor rescue when injected directly into the eyes of two commonly used models of retinal degeneration: RCS rats, with inherited degeneration, and light-damaged rats prior to bright light exposure. As was found in the previous cell culture studies, LEDGF increased production of heat shock proteins in the retina, providing a possible mechanism for cellular protection.
Oxygen Windows in ROP
Electroretinograms and retinal histology were obtained from rats exposed to hyperoxia at various time intervals following birth by Dembinska et al. (p. 1111). This regimen caused a marked reduction in the amplitude of the ERG b-wave, the number of horizontal cells, as well as in the thickness of the outer plexiform layer. These changes were found to be more severe when oxygen exposure occurred during the second week of life compared to the first. Knowledge of this critical “window” of oxygen hypersensitivity might prove instrumental in developing new therapeutic avenues to prevent the occurrence of retinopathy of prematurity.
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