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Myocilin/TIGR was the first molecule discovered to be linked with primary open-angle glaucoma (POAG), a blinding disease characterized by progressive loss of retinal ganglion cells. Mutations in myocilin/TIGR have been associated with age of disease onset and severity. The function of myocilin/TIGR and its role in glaucoma is unknown. Myocilin/TIGR has been studied in the trabecular meshwork to determine a role in regulation of intraocular pressure. The site of damage to the axons of the retinal ganglion cells is the optic nerve head (ONH). Myocilin/TIGR expression was examined in fetal through adult human optic nerves, as well as in POAG. Myocilin/TIGR was expressed in the myelinated optic nerve of children and normal adults, but not in the fetal optic nerve before myelination. Also examined was the expression in monkeys with experimental glaucoma. The results demonstrate that ONH astrocytes constitutively express myocilin/TIGR in vivo in primates. Nevertheless, myocilin/TIGR is apparently reduced in glaucomatous ONH. The colocalization of myocilin/TIGR to the myelin suggests a role of myocilin/TIGR in the myelinated optic nerve.
Dr C.S. Ricard, Department of Ophthalmology, Saint Louis University Eye Institute, 1755 Grand Boulevard, St Louis, MO 63184, USA. ricardc@slu.edu
2.15 Optic nerve (Part of: 2 Anatomical structures in glaucoma)