MMP9 is involved in glycation end-products induced increase of retinal vascular permeability in rats and the therapeutic effect of minocycline.

Author(s): Chen YD, Xu X, Xia X, Wu H, Liu K, Zheng Z, Zhu D

Affiliation(s): Department of Ophthalmology, The First People's Hospital Affiliated to Shanghai Jiao Tong University, Shanghai, China.

Publication date & source: 2008-11, Curr Eye Res., 33(11):977-83.

Publication type:

PURPOSE: To determine the role of matrix metalloproteinase 9 (MMP9) in advanced glycation end-products (AGEs) induced damage to blood-retinal barrier (BRB) and the therapeutic effects of minocycline, an MMP inhibitor, against the BRB damages. METHODS: Forty-eight Sprague Dawley rats were randomly assigned to 3 groups (16/group): A control group treated with bovine serum albumin (BSA), an AGE-BSA treated group, and a group treated with minocycline after AGE-BSA treatment. The retinas of all the animals were collected 2 weeks after treatment, and the levels of MMP9 protein and mRNA were detected by Western blotting, immunohistochemistry, and semi-quantitative RT-PCR. The permeability of retinal vessels was bio-assayed using the Evans Blue method. The correlation between the vessel permeability and the MMP9 protein levels was analyzed. RESULTS: Compared with the BSA control group, the expression of retinal MMP9 mRNA and protein were significantly increased in the AGE-BSA group, and the retinal vascular permeability was also increased in the AGE-BSA group. After the minocycline treatment, the MMP9 expression was decreased sharply and the abnormal vascular permeability was improved. There was a significant correlation between the MMP9 expression and retinal vascular permeability. CONCLUSION: MMP9 is involved in the AGE-induced retinal damage of vascular permeability, and the abnormal permeability can be partially reversed by treatment with minocycline.