Cellular senescence in the glaucomatous outflow pathway.
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.
Liton
Paloma B
PB
Department of Ophthalmology, Duke University, Erwin Road, Box 3802, Durham, NC 27710, USA. liton001@notes.duke.edu
Challa
Pratap
P
Stinnett
Sandra
S
Luna
Coralia
C
Epstein
David L
DL
Gonzalez
Pedro
P
D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000032:analysis; D016022:Case-Control Studies; D002452:Cell Count; D016922:Cellular Senescence; D003315:Cornea / Q000201:enzymology / Q000473:pathology; D005123:Eye / Q000201:enzymology / Q000473:pathology*; D005902:Glaucoma, Open-Angle / Q000201:enzymology / Q000473:pathology*; D006801:Humans; D008856:Microscopy, Fluorescence; D012590:Sclera / Q000201:enzymology / Q000473:pathology; D013194:Staining and Labeling; D018709:Statistics, Nonparametric; D014822:Vitreous Body / Q000201:enzymology / Q000473:pathology; D001616:beta-Galactosidase / Q000032:analysis*
D015415:Biomarkers; D001616:beta-Galactosidase