Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344329 (collapse)
28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Buttons obtained by trephination from both eyes of a 44-year-old myopic man with pigmentary glaucoma were studied by light and electron microscopy. Although clinically both eyes exhibited heavy pigmentation of the trabecular meshwork in the whole circumference, microscopically the trabecular meshwork of the left eye contained more pigment granules than that of the right eye, which appeared relatively acellular with collapse of the trabecular sheets. In both eyes endothelial cells covering the trabecular sheets were filled with pigment and showed various stages of degeneration. The intertrabecular spaces contained free pigment granules as well as cell debris. These observations suggest that plugging of the trabecular spaces by pigment and cell debris together with fragmentation and collapse of trabecular sheets contribute to the decrease in the facility of outflow that occurs in pigmentary glaucoma.
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PMID:The outflow tract in pigmentary glaucoma: a light and electron microscopic study. 86 44

Trabeculectomy specimens from three patients with pigmentary glaucoma were investigated electron-microscopically. The pigment accumulations were highest in the uveal and inner corneoscleral trabecular meshwork. The outer lamellae and the cribriform region were hypochromic, while the endothelium of Schlemm's canal was unpigmented. The aqueous pathways of the inner trabecular meshwork were obstructed by hyperpigmented cells, cellular fragments and released pigment granules, those of the outer trabecular meshwork by depositions of extracellular material and collagen, by degenerative cells and by collapse of the trabecular lamellae.
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PMID:[Electron microscopy studies of the trabecular meshwork in pigmentary glaucoma]. 741 49

Since its initial description over 50 years ago as a rare clinical entity, pigmentary glaucoma has become recognized as one of the most common forms of secondary open-angle glaucoma. Pigmentary glaucoma affects a much younger patient population than most other forms of open-angle glaucoma, and has a predilection for Caucasian males with myopia. Hallmarks of this disease include midperipheral iris transillumination defects, Krukenberg spindles and a heavily pigmented trabecular meshwork. The mechanism of pigment dispersion appears to be a rubbing between iris pigment epithelium and packets of lens zonules, possibly associated with an inherent abnormality of the pigment epithelium, and the mechanism of aqueous outflow obstruction is believed to involve accumulation of the pigment granules in the trabecular meshwork, followed by denudation, collapse, and sclerosis of the trabecular beams. Current management includes standard antiglaucoma drugs, laser trabeculoplasty, and filtering surgery, although research suggests the possibility of earlier intervention with medication or surgery to arrest the pigment dispersion and reverse or prevent the secondary glaucoma.
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PMID:Current concepts in pigmentary glaucoma. 809 5

The presence of the evacuation paths of aqueous humor at the level of the camerular angle makes it play an important role on open angle glaucoma pathology. The fundamental element in the evacuation of aqueous humor is the endothelial cell, who has a main contribution to the routing of aqueous humor using the phenomenon called micropinocytosis. With the age the number of endothelial cells diminishes, their function reduces and an atypical collagen appears, together with the thickness of the basal membrane, the agglutination of the trabecular blades and Schlemm channel collapse. The fact is that the raise of the evacuation resistance in open angle glaucoma must not be interpreted mechanically; a research from a biochemical and molecular point of view must be completed.
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PMID:[The resistance to drainage of the aqueous humor]. 828 12

The etiology of primary open angle glaucoma, a leading cause of age-related blindness, remains poorly defined, although elevated intraocular pressure (IOP) contributes to the disease progression. To better understand the mechanisms causing elevated IOP from aqueous humor circulation, we pursued proteomic analyses of trabecular meshwork (TM) from glaucoma and age-matched control donors. These analyses demonstrated that Cochlin, a protein associated with deafness disorder DFNA9, is present in glaucomatous but absent in normal TM. Cochlin was also detected in TM from the glaucomatous DBA/2J mouse preceding elevated IOP but found to be absent in three other mouse lines that do not develop elevated IOP. Histochemical analyses revealed co-deposits of Cochlin and mucopolysaccharide in human TM around Schlemm's canal, similar to that observed in the cochlea in DFNA9 deafness. Purified Cochlin was found to aggregate after sheer stress and to induce the aggregation of TM cells in vitro. Age-dependent in vivo increases in Cochlin were observed in glaucomatous TM, concomitant with a decrease in type II collagen, suggesting that Cochlin may disrupt the TM architecture and render components like collagen more susceptible to degradation and collapse. Overall, these observations suggest that Cochlin contributes to elevated IOP in primary open angle glaucoma through altered interactions within the TM extracellular matrix, resulting in cell aggregation, mucopolysaccharide deposition, and significant obstruction of the aqueous humor circulation.
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PMID:Proteomics reveal Cochlin deposits associated with glaucomatous trabecular meshwork. 1557 65