Abstract
Lumican serves an important role in the maintenance of sclera biomechanical properties. However, whether lumican expression is altered in myopia and the mechanisms of action involved are unknown. In the present study, the expression of lumican in cultured scleral fibroblasts and in the scleral tissue of a rat model of form-deprivation myopia was assessed. It was confirmed that diopter was decreased, whereas axial length was increased in modeled eyes relative to normal control eyes, indicating that the model of myopia was successfully established. These pathologic changes were accompanied by the upregulation of lumican and tissue inhibitor of metalloproteinases (TIMP)-2, as well as the downregulation of matrix metalloproteinase (MMP)-2 and MMP-14. The same trends in TIMP-2, MMP-2 and MMP-14 expression were observed when lumican was overexpressed in cultured scleral fibroblasts. Additionally, cell proliferation decreased whereas apoptosis increased compared with those of control cells. Inhibiting lumican expression had no effect on cell proliferation or apoptosis, but stimulated the expression of MMP-2 and MMP-14 while decreasing that of TIMP-2. The results suggested that lumican overexpression contributed to myopia by promoting apoptosis in scleral fibroblasts via the modulation of TIMP-2, MMP-2 and MMP-14 expression.