Abstract
Abstract: :
Purpose:The trabecular meshwork is a main passageway for aqueous humor. Its abnormal function can lead to the blockage of aqueous and cause intraocular pressure (IOP) to increase, resulting in glaucoma. In this study, we investigate the expression of AQP1 in trabecular meshwork cells of primary glaucoma patients. Methods:Trabecular meshwork tissues were taken during trabeculectomy surgery in primary glaucoma patients who were divided into 4 groups: G1: primary chronic open-angle glaucoma; G2: primary acute angle-closure glaucoma (early onset); G3: primary chronic angle-closure glaucoma; G4 primary glaucoma of advanced-stage. For a control group (GC) we used eyes from donors without ocular disease. The frozen sections of the trabeculectomy specimens were HE stained for the structural study, and were also used for immunohistochemical analysis. Results:Comparing to the normal trabecular meshwork, we have found structure disruption, extra-cellular matrix accumulation, meshwork atrophy, and fibrous hyperplasia in G1, G3 and G4 groups. We have counted the numbers of trabecular meshwork endothelial cells (counted the numbers of nucleus stained in blue within 3 fields, 400 X) between different groups and we have found that they were in this order: GC: 89.0 ± 4.6; G2: 87.5 ± 4.1; G3: 59.6 ± 5.2; G1: 47.9 ± 5.0 and G4: 45.9 ± 4.4. Except for G2, the numbers of endothelial cells in the other 4 Groups were decreased significantly (P<0.01). In the immunohistochemical study, we found dark brown particles in the membranes of trabecular meshwork endothelial cells in all of groups, which represented AQP1 positive expression. We counted the numbers of these positive dark brown articles within 10 fields (400 X) and found that expression of AQP1 in group G2 (34.3 ± 4.1) was higher than that in group GC (28.8 ± 3.1, P<0.05), while the expression of AQP1 in the other three glaucoma groups (G1: 6 ± 2.39; G3: 7.3 ± 2.4 and G4: 6 ± 2.9) was much less than that of GC (P<0.05). Conclusions: Our results indicate that persistent high IOP can destroy the trabecular meshwork structure and decrease the number of the endothelial cells in it, and the expression of AQP1 in these cells was decreased. However, the expression of AQP1 in trabecular meshwork cells can be accommodated when IOP rises sharply in the early state.
Keywords: immunohistochemistry • trabecular meshwork • microscopy: light/fluorescence/immunohistochem