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C.–K. Joo, K.–S. Lee, J. Lyu; Insulin Enhances Cell Migration Through EGFR in Human Corneal Epithelial Cells . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5031.
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© ARVO (1962-2015); The Authors (2016-present)
The mechanism of the induction of signals respond to insulin is not fully elucidated, although numerous studies have been suggested that cornea wound healing is, at least in part, mediated by insulin. This study focused on identifying the mechanism of insulin signal pathway.
SV40–immortalized human corneal epithelial (THCE) cells were cultured in growth factors– and serum–free medium on a diluted Matrigel matrix, which is similar to basement membrane of corneal epithelium. Wound was introduced with a micropipette tip. Closure of the scratch wound was photographed at 12 hrs after exposed to insulin. The activation of epidermal growth factor recptor (EGFR) was analyzed with immunoprecipition. Cytoskeletal rearrangement was also determined with rhodamin–congugated phalloidin.
Exposure of corneal epithelial cells to insulin induce the phosphorylation of EGFR. Inhibition of EGFR activation by AG1478 also reduced the phosphorylation of insulin–induced ERK. The wound closure in present of insulin was delayed by the inhibition of EGFR. In addition, cells exposed to insulin displayed stress fiber along with depletion of submembranous cortical actin while cells in the presence of AG1478showed the submembranous cortical actin and few fine fibrils.
The inhibition of EGFR activity decreased cell migration in insulin–induced wound repair, an effect that was mimicked by the inhibition of MMP activation. The inhibition of MMP activity showed a decreased EGFR phosphorylation. These data provided evidence that insulin involve in wound healing of corneal epithelium through the activation of EGFR, and emphasize a new molecular mechanism for the insulin signal pathway in the process of corneal wound healing.
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