[No authors listed]
Hepatocyte growth factor (HGF) and keratinocyte growth factor (KGF), two paracrine growth factors, modulate corneal epithelial cell metabolism, apoptosis and survival. Vascular endothelial growth factor (VEGF) serves as a proangiogenic factor in corneal neovascularization (CNV), which is a major cause of vision impairment and corneal blindness. The aim of the present study was to evaluate the ability of HGF and KGF to influence VEGF and its receptor, kinase insert domain receptor (Flkâ1) in corneal injury and CNV in rats induced by ultraviolet radiation (UVR). An UVRâinduced corneal injury rat model was successfully established to characterize the expression patterns of KGF, HGF, VEGF and Flkâ1 in corneal tissues. Corneal epithelial cells were extracted and treated with small interfering RNAs (siRNAs) targeting KGF, HGF or both (siâKGF, siâHGF or siâHGF/KGF). The effects of HGF and KGF were examined through detection of the expression of KGF, HGF, VEGF and Flkâ1, and the evaluation of cell proliferation, cell cycle and cell apoptosis. The expression levels of KGF, HGF, VEGF and Flkâ1 in corneal tissues were increased in the rat model. In the cell experiments, the transfection of siâHGF/KGF resulted in reductions in VEGF, Flkâ1, KGF and HGF. In addition, decreased cell proliferation and elevated cell apoptosis were found in the corneal epithelial cells from the rat model following KGF and HGF gene silencing. Taken together, these findings suggest that HGF and KGF gene silencing inhibits UVRâinduced corneal epithelial proliferation and CNV and may function as novel targets for corneal wound healing.
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