Gene Expression Analysis of Matrix Metalloproteinase 2, Matrix Metalloproteinase 13 and Tissue Inhibitor of Matrix Metalloproteinase 1 in Epithelium of Diseased Human Corneas*

It has been shown in animal models that matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) are responsible for remodelling and neovascularization of the diseased cornea. Under normal conditions, MMPs are expressed at relatively low levels, which may increase in case of different corneal diseases. In this paper we have investigated gene expression of matrix metalloproteinase 2, matrix metalloproteinase 13 and their inhibitor TIMP-1, in keratoconus, bullous keratopathy and vascularized corneal scar; aiming to determine whether these molecules are differentially expressed in epithelium of diseased human corneas. Keratoconus, bullous keratopathy and vascularized corneal scar were chosen for two reasons: they represent low-, intermediateand high-risk corneal disease regarding corneal graft rejection rate (respectively) and they are very common reason for corneal transplantation. Our results have show that in bullous keratopathy, expression of both MMP-13 and MMP-2 genes were significantly increased compared to vascularized corneal scar and keratoconus; however only MMP-13 reached significance in our relatively small human sample. These results are comparable to our previously published data on protein levels of MMPs in diseased human corneal epithelium, where we showed significant increase of MMP-13 and MMP-2 proteins in patients with bullous keratopathy compared to keratoconus. TIMP-1 gene expression remained constant across all groups of patients, impli-