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Abstract #15738 Published in IGR 2-3
Ultrastructural localization of myocilin in human trabecular meshwork cells and tissues
Ueda J; Wentz-Hunter KK; Cheng EL; Fukuchi T; Abe H; Yue BYJournal of Histochemistry and Cytochemistry 2000; 48: 1321-1330
The authors examined ultrastructurally the localization of myocilin (formerly called trabecular meshwork inducible glucocorticoid response, or TIGR) protein in cultured human trabecular meshwork (TM) cells and in normal human TM tissues. The TM, a specialized tissue located at the chamber angle of the eye, is believed to be responsible for the development of glaucoma. The myocilin gene has been directly linked to both juvenile and primary open-angle glaucomas, and multiple mutations have been identified. Human TM cells were treated with 0.1 mM of dexamethasone (DEX) to induce myocilin expression. This protein was immunolocalized by colloidal gold electron microscopy using an anti-human myocilin polyclonal antibody. Double labelling with different sizes of gold particles was also performed with additional monoclonal antibodies specific for cell organelles and structures. In both DEX-treated and untreated cultured cells, myocilin was associated with mitochondria, cytoplasmic filaments, and vesicles. In TM tissues, myocilin was localized to mitochondria and cytoplasmic filaments of TM cells, elastic-like fibers in trabecular beams, and extracellular matrices in the juxtacanalicular region. These results indicate that myocilin is localized both intracellularly and extracellularly at multiple sites. This protein may exert diverse biological functions at different sites.
Dr. J. Ueda, Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago College of Medicine, Chicago, IL 60612, USA
Classification:
1.2 Population genetics (Part of: 1 General aspects)
2.5 Meshwork (Part of: 2 Anatomical structures in glaucoma)
4 Tissue culture of ocular cells
