Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of sialic acid moieties in the trabecular wall of Schlemm's canal in normal human and monkey eyes, as well as in limited tissue samples from patients with primary open-angle glaucoma (POAG), was investigated by using polycationic ferritin (PCF) at varying pH and colloidal iron at pH 1.8. At pH 1.8-1.9, both PCF and colloidal iron labeled the luminal surface of the endothelial cells of Schlemm's canal in normotensive monkey and human eyes, whereas binding was sparse and random on the basal surface. At a pH of 3.3 and higher, PCF showed increased binding that was confirmed exclusively to the luminal surface of the cells. In trabeculectomy tissue samples from eyes with POAG, PCF at pH 1.9 showed a greater density of labeling on both the basal and luminal cell surfaces, as well as in the subendothelial region, than was observed in normotensive eyes. Given the fact that sialic acid is a moiety which stabilizes cell membranes, we suggest that in normal eyes the absence of sialated molecules on the basal cell surface leaves 'receptor' sites for the initiation of the macrovacuolation process which allows the bulk outflow of aqueous humor across the endothelial barrier of Schlemm's canal. Our preliminary observations in glaucomatous eyes indicate a loss of such receptor sites, which may account for the depletion of macrovacuolar configurations in cases of advanced POAG. Our discussion relates these findings to the pathogenesis of POAG and to the possible role for a defective transmembrane interaction of the surface glycoproteins (fibronectin and laminin) with the cytoskeleton of the endothelial cells lining Schlemm's canal and the cells in the pericanalicular tissue.
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PMID:Localization of sialic acid moieties in the endothelial lining of Schlemm's canal in normal and glaucomatous eyes. 358 14

Iron is essential for many metabolic processes but can also cause damage. As a potent generator of hydroxyl radical, the most reactive of the free radicals, iron can cause considerable oxidative stress. Since iron is absorbed through diet but not excreted except through menstruation, total body iron levels buildup with age. Macular iron levels increase with age, in both men and women. This iron has the potential to contribute to retinal degeneration. Here we present an overview of the evidence suggesting that iron may contribute to retinal degenerations. Intraocular iron foreign bodies cause retinal degeneration. Retinal iron buildup resulting from hereditary iron homeostasis disorders aceruloplasminemia, Friedreich's ataxia, and panthothenate kinase-associated neurodegeneration cause retinal degeneration. Mice with targeted mutation of the iron exporter ceruloplasmin have age-dependent retinal iron overload and a resulting retinal degeneration with features of age-related macular degeneration (AMD). Post mortem retinas from patients with AMD have more iron and the iron carrier transferrin than age-matched controls. Over the past 10 years much has been learned about the intricate network of proteins involved in iron handling. Many of these, including transferrin, transferrin receptor, divalent metal transporter-1, ferritin, ferroportin, ceruloplasmin, hephaestin, iron-regulatory protein, and histocompatibility leukocyte antigen class I-like protein involved in iron homeostasis (HFE) have been found in the retina. Some of these proteins have been found in the cornea and lens as well. Levels of the iron carrier transferrin are high in the aqueous and vitreous humors. The functions of these proteins in other tissues, combined with studies on cultured ocular tissues, genetically engineered mice, and eye exams on patients with hereditary iron diseases provide clues regarding their ocular functions. Iron may play a role in a broad range of ocular diseases, including glaucoma, cataract, AMD, and conditions causing intraocular hemorrhage. While iron deficiency must be prevented, the therapeutic potential of limiting iron-induced ocular oxidative damage is high. Systemic, local, or topical iron chelation with an expanding repertoire of drugs has clinical potential.
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PMID:Iron homeostasis and toxicity in retinal degeneration. 1792 Oct 41