Cellular senescence in the glaucomatous outflow pathway

• DOI: 10.1016/j.exger.2005.06.005
• Publication Date: 2005-07-28T21:24:29Z
• Authors: Paloma B. Liton; Pratap Challa; Sandra Stinnett; Coralia Luna; David L. Epstein; Pedro Gonzalez
• Keywords: Aged, 80 and over; Staining and Labeling; Cell Count; Eye; beta-Galactosidase; Statistics, Nonparametric; Cornea; Vitreous Body; 03 medical and health sciences; 0302 clinical medicine; Microscopy, Fluorescence; Case-Control Studies; Humans; Biomarkers; Cellular Senescence; Glaucoma, Open-Angle; Sclera; Aged

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-beta-galactosidase (SA-beta-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-beta-gal positive cells. These results suggest a potential role for cellular senescence in the pathophysiology of the outflow pathway.