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Xinyi Wu; Downregulation of IGF-1 decreased proliferation, migration and increased apoptosis in diabetes-impaired corneal epithelial wound healing. Invest. Ophthalmol. Vis. Sci. 2014;55(13):4680.
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To investigate the expression, function and mechanism of IGF-1 in diabetes-impaired corneal epithelial wound healing.
The effects of high glucose on IGF-1 and IGF-1R expression were assessed in injured Telomerase-immortalized human corneal epithelial (THCE) cells and wounded corneal epithelium of streptozotocin induced diabetic rats by RT-PCR, ELISA, western blot or immunofluorescence. The effects of IGF-1 in the presence of high glucose on cell proliferation, migration and apoptosis were evaluated by MTT, scratch assays in vitro and flow cytometry. The possible molecular mechanisms were detected by the levels of ki-67, MMP-2, bax, and bcl-2 expression using RT-PCR, immunohistochemistry or western blot.
Delayed epithelial wound healing was observed in injured THCE cells cultured in high glucose and wounded corneal epithelium of diabetic rats which were accompanied with reduced IGF-1 and IGF-1R mRNA and protein expression. High glucose impaired THCE cells proliferation, migration and increased apoptosis via downregulating ki-67, MMP-2, bcl-2 and upregulating bax mRNA and protein expression. Treatment with IGF-1 reversed these high glucose effects.
Delayed epithelial wound healing in diabetic corneas might result, at least in part, from impaired IGF-1/IGF-1R system and consequently decreased cell proliferation, migration and increased cell apoptosis.
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