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. 2005 Aug-Sep;40(8-9):745-8.
doi: 10.1016/j.exger.2005.06.005.

Cellular senescence in the glaucomatous outflow pathway

Paloma B Liton  1 , Pratap Challa, Sandra Stinnett, Coralia Luna, David L Epstein, Pedro Gonzalez
Affiliations

Cellular senescence in the glaucomatous outflow pathway

Paloma B Liton et al. Exp Gerontol. 2005 Aug-Sep.

Abstract

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.

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Figures

Fig. 1
Fig. 1
Analysis of markers for cellular senescence in the outflow pathway of non-glaucomatous and POAG donor eyes. (A) Photographs of the anterior segments from a non-glaucomatous control and a POAG stained for SA-β-galactosidase activity. (B) Presence of SA-β-gal stained cells in cross sections from a control and POAG donor (above), and DAPI staining of the same sections (below). These results are representative of six controls and six POAG eyes analyzed.
See this image and copyright information in PMC

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