bromochloroacetic-acid and Glaucoma

In an experimental autoimmune animal model, retinal ganglion cell (RGC) loss was induced through immunization with glaucoma-related antigens. The target of this study was to investigate the pathomechanism behind this decline and the serum antibody reactivity against ocular and neuronal tissues after immunization with glaucoma- and non-glaucoma-associated antigens.. Rats immunized with optic nerve antigen homogenate (ONA) or keratin (KER) were compared to control rats (CO). Intraocular pressure (IOP) was measured, and the fundi were examined regularly. Four weeks afterward, cells were counted in retinal flat mounts. Retina, optic nerve, and brain sections from healthy animals and optic nerve sections from immunized animals were incubated with serum collected at different time points. The occurrence of autoreactive antibodies was examined. Signs of antibody deposits, microglia activation, and demyelination were sought in optic nerves of immunized animals. Brain sections were examined for abnormalities.. No IOP or fundus changes were observed. Animals immunized with ONA showed a significant cell loss compared with the CO group. Elevated autoreactive antibodies against retina, optic nerve, and brain were observed. Animals immunized with KER, despite their immunologic response against KER, demonstrated neither RGC loss, nor increased development of autoreactive antibodies. Optic nerve from animals immunized with ONA demonstrated antibody accumulation, glia activation, and demyelination. No such observations were made in the KER or CO groups. Brain sections were without pathologic findings.. Systemic autoimmunity against ocular and neuronal epitopes, mediated by accordant autoreactive antibodies, is involved in the inflammatory processes that cause RGC degeneration in this experimental animal model.

Topics: Animals; Autoantibodies; Brain; Demyelinating Diseases; Disease Models, Animal; Epitopes; Glaucoma; Immunization; Immunoglobulin G; Intraocular Pressure; Keratins; Male; Microglia; Nerve Degeneration; Nerve Tissue Proteins; Optic Nerve; Rats; Rats, Inbred Lew; Retinal Ganglion Cells

As cell cultures of pericytes derived from bovine retina are in regular use by a number of investigators, we decided to confirm the identity of these cells, to show them different from other cells that might contaminate cultures derived from retinal tissue, to characterize the properties they share with pericytes in situ and to establish a practical and effective means for confirmation of the cell type of each batch of cultured cells used in scientific studies. Cultured pericytes differed in immunocytochemical reactions and phagocytic properties from vascular smooth muscle, vascular endothelial cells, astroglia, conjunctival fibroblasts or retinal pigment epithelium. Like vascular smooth muscle, pericytes in situ and those in culture have the contractile proteins actin and myosin, which implies a potential role in blood flow control. In routine studies of cultured pericytes, they can be identified by their unique reaction in situ and in vitro with the antiganglioside monoclonal antibody 3G5. The presence of any contaminating endothelial cells can be recognized by their ability to take up acetylated low-density lipoprotein.

Topics: Animals; Antibodies, Monoclonal; Blood Flow Velocity; Capillaries; Cattle; Cells, Cultured; Contractile Proteins; Desmin; Endothelium, Vascular; Fluorescent Antibody Technique, Indirect; Gangliosides; Glaucoma; Keratins; Microscopy, Fluorescence; Muscle, Smooth, Vascular; Retinal Vessels

A 29-year-old woman had unilateral essential iris atrophy, corneal endothelial changes, and absolute glaucoma. The enucleated eye was examined by routine light microscopy. Separate portions of unfixed fresh frozen cornea were sectioned and reacted with monoclonal antibodies against keratins, vimentin, and inflammatory cell markers. Stains for filamentous actin (f-actin) were performed using the 7-nitro-benz-2-oxa-1,3-diazolylphallacidin (NBD phallacidin) probe. In addition, portions of cornea and iris were examined by scanning and transmission electron microscopy. Immunocytochemical stains with anti-keratin antibodies showed reactivity only in the corneal epithelium of the patient and normal control. Immunoreactivity with anti-vimentin antibodies was observed in corneal endothelium and keratocytes of the patient and control, but was negative in the epithelium. Staining for f-actin appeared more pronounced in the corneal endothelium of the patient. Scanning electron microscopy of the corneal endothelium showed irregularity in cell size and shape and filopodial processes characteristic of migrating cells. Transmission electron microscopy disclosed abnormalities of Descemet's membrane and endothelium with a posterior collagenous layer. The corneal endothelium displayed normal junctional complexes without desmosomal junctions or increased microvillus projections. Increased 10-nm cytoplasmic filaments were noted consistent with the expression of vimentin. Occasional chronic inflammatory cells perturbed the corneal endothelium and were detected within the endothelial layer. Alterations in the endothelium and Descemet's membrane suggest the acquired nature of this disease.

Topics: Actins; Adult; Atrophy; Corneal Diseases; Endothelium, Corneal; Female; Glaucoma; Humans; Immunohistochemistry; Iris; Iris Diseases; Keratins; Microscopy, Electron; Microscopy, Electron, Scanning; Syndrome