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| April 2006 | Inside IOVS | Volume 47/4 |
Keratin 12-Positive Cells Are Present in Conjunctival and Corneal Epithelium
Expression of keratin 12 (K12) has been considered a hallmark of cornea-type differentiation. Kawasaki et al. (p. 1359) present evidence that K12-positive cells reside even in conjunctival epithelium. Additionally, they indicate that such cells have almost the same gene expression pattern as corneal epithelial cells. Moreover, these cells seem to have their own stem cells just beneath them. These results strongly suggest that the K12-positive cells in conjunctival epithelium are ectopically residing corneal epithelial cells.
Superoxide Signals Apoptosis in Retinal Ganglion Cells
Axonal damage to retinal ganglion cells (RGCs) occurs in glaucoma and other optic neuropathies, and results in apoptotic death. Lieven et al. (p. 1477) demonstrate that axonal injury induces a burst of superoxide in the RGC cell body, serving as an early signal for apoptosis. The burst is not inhibited by neurotrophic factors and appears to be generated in mitochondria. This raises the possibility that interfering with activation of a superoxide signaling pathway could be a neuroprotective strategy for optic nerve diseases.
A Distinct Glycogene Expression Pattern in POAG Trabecular Meshwork
Diskin et al. (p. 1491) analyzed gene expression patterns of whole normal and primary open angle glaucomatous (POAG) trabecular meshwork tissues using a specific microarray focused on glycogenes – genes involved in carbohydrate-mediated recognition systems. The authors found a distinct "signature" shared by POAG tissues but not by normal trabecular meshwork. Specific genes that were found to be elevated in POAG tissues include cell adhesion molecules that may, in the future, be used as diagnostic markers for the disease, as well as genes involved in extracellular matrix processing, which has been shown to be different between normal and POAG tissues.
Blocking the p38 Signaling Pathway: A Potential New Adjunct to Glaucoma Surgery
Postoperative scarring persists as the most important problem in fistulating glaucoma surgery. Current standard antimetabolite treatment is limited by its lack of specificity and ensuing side effects on ocular surface and conjunctiva. Meyer-ter-Vehn et al. (p. 1500) investigated intracellular signaling pathways involved in TGF-b-driven ocular scarring. Specific pharmacological inhibition of the p38 signaling pathway by small molecular inhibitors prevents myofibroblast transdifferentiation in vitro and may provide a new strategy for specific antifibrotic therapy after glaucoma surgery.
Antibodies to Galectin-1 as Prognostic Markers for Uveitis
Uveitis is a generic term that encompasses a variety of intraocular inflammatory responses of infectious or autoimmune origin. Despite considerable progress in elucidating the immunopathogenesis of these ocular disorders, there is still scarce information about reliable immunological markers of disease evolution. Galectin-1, an endogenous lectin found at sites of activation and immune privilege, plays a critical role in the regulation of the immune response. The results presented by Romero et al. (p. 1550) highlight the clinical importance of specific anti-retinal galectin-1 antibodies in sera from patients with autoimmune and infectious uveitis, indicating their potential prognostic use for the follow-up of inflammatory ocular diseases.
Oxygen and the Lens
Exposure to elevated oxygen is a risk factor for nuclear cataracts. Shui et al. (p. 1571) mapped the oxygen distribution in the rabbit eye and calculated the rate of oxygen consumption by the posterior of the lens in vivo. Oxygen levels were low around the lens near the ciliary folds and in the anterior chamber angle. Intraocular oxygen levels and consumption by the lens increased greatly when animals breathed more oxygen. Oxidative damage to lens proteins and lipids may result from increased levels of free radicals generated by oxidative metabolism. Maintaining low oxygen levels around the lens may protect against nuclear cataracts.
A Lipid Molecule Activates Photoreceptor Death
The death of photoreceptors leads to many retina neurodegenerative diseases that cause blindness and have no treatment yet. The precise pathways that induce this death are still ill-defined. German et al. (p. 1658) show that the increase in the intracellular levels of a lipid molecule, ceramide, activates photoreceptor apoptosis, while blocking this increase precludes photoreceptor death upon different situations of cellular stress. This suggests that ceramide is a key activator of photoreceptor apoptosis and searching for ways to keep ceramide levels low might provide useful therapeutic tools for preventing photoreceptor death in neurodegenerative diseases.
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