Abstract
BackgroundTo investigate the expression of Matrix Metalloproteinases 2 and aquaporin-1 in corneoscleral junction and explore the mechanism of trabecular damageafter angle-closure.MethodsThirty New Zealand white rabbits were randomly assigned into 2 groups, theexperimental group (Group 1) including twenty five rabbits and the control group (Group 2) including 5 rabbits. The rabbits in the experimental group were used to establish angle-closure models, and the rabbits in the control group were not subjected to any operation. All the rabbits were followed by slit lamp microscopy, Tonopen tonometer, and anterior segment optical coherent tomography (AS-OCT). The expressions of metalloproteinase MMP-2, aquaporin-1, and tissue inhibitors of metalloproteinase-2 in corneoscleral junctionwere evaluatedin both groups byimmunofluorescence, quantitative reverse-transcription polymerase chain reaction (qRT-PCR), and enzyme-linked immunosorbent assay (ELISA).ResultsSlit-lamp examination showed that angle-closure model was successfully established in twenty rabbits. The extent of angle-closure was about 2 to 4 clock hours in all the rabbit models, but the intraocular pressure (IOP) of the rabbits distributed from 8.57 to 15.25 mmHg and no significant high IOP was found in the follow-up period. The AQP-1-positive cells mainly located in Schlemm’s canal, the inner surface of trabecular meshwork (TM), and the surface of iris, which began to decline on 1 month after angle-closure. MMP2 staining was diffuse in trabecular meshwork and iris. Immunofluorescence signal of MMP2 was strong within 1 month after angle-closure, and subsequently became weak. qRT-PCR and ELISA showed that the expression of MMP-2 and TIMP-2 increased within 1 month after angle-closure and then declined gradually. The AQP-1 levels showed slightly declined on 1 month after angle-closure.ConclusionsAltered levels of MMPs, TIMPs, and AQP-1 were found in the area of angle-closure, which may be involved in the damage of TM and Schlemm’s canal after angle-closure.
Highlights
To investigate the expression of Matrix Metalloproteinases 2 and aquaporin-1 in corneoscleral junction and explore the mechanism of trabecular damageafter angle-closure
Goniosynechialysis has been reported to be an effective therapy for chronic angle-closure glaucoma by separation of peripheral anterior synechiae and showed fewer postoperative
Studies regarding the changes of trabecular meshwork (TM) and s canal (SC) after angle-closure may hold a great significance for revealing the pathogenesis of Angle-closure glaucoma (ACG)
Summary
To investigate the expression of Matrix Metalloproteinases 2 and aquaporin-1 in corneoscleral junction and explore the mechanism of trabecular damageafter angle-closure. Angle-closure glaucoma (ACG) is a major cause of blindness worldwide and is characterized by increased intraocular pressure (IOP) due to appositional or synechial angle closure associated with visual field defects [1]. Goniosynechialysis has been reported to be an effective therapy for chronic angle-closure glaucoma by separation of peripheral anterior synechiae and showed fewer postoperative. Jiang et al BMC Ophthalmology (2019) 19:43 of ECM within the JCT have been identified as one of the main causes of the increasing IOP in primary open-angle glaucoma (POAG). MMPs have a vital role in ECM degradation and remodeling in the TM, which maintains the outflow pathway and IOPhomeostasis [8]. It was reported that MMP-2 levels were increased in POAG cases [7]. The change of MMP-2 level after angle-closure was still not reported
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