Plasminogen activator inhibitor-1 in the aqueous humor of patients with and without glaucoma.

Objective: To determine the levels of plasminogen activator inhibitor-1 (PAI-1) and total protein in the aqueous humor of patients with glaucoma vs those without glaucoma.

Methods: A total of 125 aqueous humor samples (50-150 microL each) were collected at 3 institutions from patients with glaucoma and a control group of patients with cataract. Fifteen samples were excluded, and the levels of PAI-1 antigen were determined by enzyme-linked immunosorbent assay in 110 samples (36 glaucoma and 74 control). Total protein levels were determined by the Bradford method in 81 samples (28 glaucoma and 53 control), in which the aqueous humor collected was sufficient. Statistical analysis of the results was conducted using the Mann-Whitney U test. The correlation between PAI-1 and protein levels was calculated using the Spearman rank correlation coefficient.

Results: The mean +/- SD PAI-1 levels detected in aqueous humor samples of the control and glaucoma groups were 0.44 +/- 0.61 and 1.45 +/- 1.91 ng/mL, respectively. The mean +/- SD levels of total protein were 64.91 +/- 89.75 and 86.64 +/- 44.16 microg/mL, respectively. For both parameters, the difference between the 2 groups was significant (P< .001). The correlation between PAI-1 and total protein levels was moderate in the glaucoma group (r = 0.43; P = .01) and low in the control group (r = 0.23; P = .04).

Conclusions: The glaucoma group showed in the aqueous humor a 3.3-fold increase in the mean level of PAI-1 compared with the control group, whereas the increase in total protein level was only 1.3-fold. These data are consistent with the possibility that intraocularly produced PAI-1 may contribute to glaucoma pathogenesis.

Clinical Relevance: Reducing the production or activity of PAI-1 in the eye could constitute a new target for the design of drugs to treat glaucoma.