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Abstract #12549 Published in IGR 7-3
Cellular senescence in the glaucomatous outflow pathway
Liton PB; Challa P; Stinnett S; Luna C; Epstein DL; Gonzalez PExperimental Gerontology 2005; 40: 745-748
See also comment(s) by Douglas Rhee • Ernst Tamm •
The mechanisms responsible for the progressive malfunction of the trabecular meshwork (TM)-Schlemm's canal (SC) conventional outflow pathway tissue in primary open angle glaucoma (POAG) are still not fully understood. To determine whether POAG is characterized by an accumulation of senescent cells, similar to what has been described in other diseases, we have compared the levels of the senescence marker senescence-associated-β-galactosidase (SA-β-gal) in the outflow pathway cells of POAG and age-matched control donors. POAG donors demonstrated a statistically significant fourfold increase in the percentage of SA-β-gal positive cells. These results suggest a potential role for cellular senescence in the pathophysiology of the outflow pathway.
Dr. P. Gonzalez, Department of Ophthalmology, Duke University, Box 3802, Erwin Road, Durham, NC 27710, USA
Classification:
2.5.1 Trabecular meshwork (Part of: 2 Anatomical structures in glaucoma > 2.5 Meshwork)
2.5.2 Schlemms canal (Part of: 2 Anatomical structures in glaucoma > 2.5 Meshwork)
3.3 Immunohistochemistry (Part of: 3 Laboratory methods)
1.3 Pathogenesis (Part of: 1 General aspects)