Human myocilin is identical to TIGR (trabecular meshwork inducible glucocorticoid response) which is responsible for the pathogenesis of juvenile-onset primary open angle glaucoma (GLC1A). We have isolated cDNA for mouse myocilin (Myoc) and investigated mouse myocilin gene expression in ocular tissues with in situ RNA hybridization. Hybridization signals were observed in the iris, ciliary body, trabecular meshwork, sclera, and retina in the mouse eye. The marked signals were seen in trabecular meshwork cells and the anterior portion of sclera. These findings suggest that myocilin mutation could affect the capacity of aqueous outflow and cause elevation of the intraocular pressure which is involved in the pathogenesis of glaucoma.
|ジャーナル||Biochemical and Biophysical Research Communications|
|出版ステータス||Published - 1998 7月 9|
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