Targeting XXXX to Treat Delayed Wound Healing in @entity1 Diabetic Organ-Cultured Corneas.

@entity1018 @entity1 @entity267 @entity6 @entity470 @entity30683 @entity1435 @entity6991 @entity446
Limbal epithelial stem cells (LESC) residing at the corneal periphery are largely responsible for maintaining corneal optical transparency by continuously supplying new corneal epithelial cells, which mature during their radial migration to the central @entity267 . @entity6 ( @entity6 ) affects all the structures of the eye including the @entity267 . Frequent @entity30683 , delayed wound @entity446 , and microbial infections are common alterations of the @entity6 eye that can result in @entity1018 . MicroRNAs (miRNAs) are short non-coding oligonucleotides that regulate gene expression by repressing translation. Our purpose was to understand the role of @entity6991 in the @entity1 limbal versus central corneal epithelial compartment in normal and pathological conditions such as @entity6 . Using quantitative real-time PCR (QPCR) we found @entity6991 enrichment in the limbal corneal compartment. This miRNA was also expressed at higher levels in the @entity6 vs. normal limbus. Cell migration and wound closure were significantly delayed in normal and @entity6 primary limbal epithelial cells (LEC) transfected with @entity6991 . Cells treated with @entity6991 had decreased levels of phosphorylated (activated) @entity1435 and @entity470 , mediators of epithelial wound @entity446 . Conversely, inhibition of @entity6991 significantly enhanced cell migration in both normal and @entity6 primary LEC and in @entity6 organ-cultured corneas by nearly 40% vs. scrambled miRNA control, accompanied by increased phosphorylated signaling intermediates. Transfection of @entity6991 in cultured LEC resulted in an increased immunoreactivity for putative LEC markers Frizzled-7 and K15, whereas inhibition of @entity6991 decreased their expressions. These data suggest that @entity6991 plays a role in LEC maintenance at the corneal periphery, and its expression is downregulated during their migration towards the central @entity267 and accompanying terminal differentiation. Furthermore, abnormal @entity6991 upregulation may be an important mechanism of delayed wound @entity6 .
