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Carboxyamido-triazole (CAI) Inhibits Sub-steps of Choroidal Neo-vascularization In Vitro
1Hoffmann S., 2He S., 3Kohn E., 2Hinton D., 2Ryan S. J., 1Wiedemann P.,
1Universität Leipzig, Klinik und Poliklinik für Augenheilkunde (Leipzig)
2Doheny Eye Institute, University of Southern California (Los Angeles)
3National Institute of Health, Signal Transduction Unit (Bethesda)
Purpose: Retinal pigmented epithelial cells (RPEs) and choroidal endothelial cells (CECs) are of importance in the process of choroidal neovascularization in exudative age related macular degeneration (AMD). In this study, we investigated the effects of CAI, a drug modulating calcium mediated signal transduction on substeps of choroidal neovascularization by RPE cells and CECs.
Methods: CAI effects on VEGF and bFGF induced CEC and RPE proliferation, cell attachment onto several extracellular matrices and fibronectin mediated migration were investigated. In addition, the effects of the drug on bFGF and VEGF induced MMP-2 secretion by CECs were investigated by zymography and MMP-2 ELISA. Furthermore, proapoptotic effects of CAIs were explored by a commercial apoptosis assay.
Results: At a concentration of 10 µM, CAI significantly inhibited serum-induced proliferation of CECs more strongly than RPE cell proliferation. However, VEGF and bFGF induced proliferation of these cells was inhibited even more effectively than serum induced proliferation. The drug also inhibited fibronectin induced migration of CECs and RPE cells and the VEGF/ bFGF stimulated MMP-2 secretion by CECs. In concentrations higher than 10 µM CAI, an apoptosis induction on RPEs and CECs was seen.
Conclusions: CAI inhibits the proliferative and invasive behavior of RPE cells and CECs including migration, cell attachment, and MMP-2 secretion by CECs. Therefore, CAI may be of value for the treatment of choroidal neovascularization in exudative AMD.