Abstract
BackgroundTo investigate effects of knockdown of epiplakin gene expression on the homeostasis of cultured corneal epithelial cell line. We previously reported acceleration of corneal epithelial wound healing in an epiplakin-null mouse.MethodsGene expression of epiplakin was knockdowned by employing siRNA transfection in SV40-immortalized human corneal epithelial cell line. Protein expression of E-cadherin, keratin 6 and vimentin was examined by western blotting. Cell migration and proliferation were examined by using scratch assay and Alamar blue assay, respectively.ResultsScratch assay and Alamar blue assay showed migration and proliferation of the cells was accelerated by epiplakin knockdown. siRNA-knockdown of epiplakin suppressed protein expression of E-cadherin, keratin 6 and vimentin.ConclusionsDecreased expression of E-cadherin, keratin 6 and vimentin might be included in the mechanisms of cell migration acceleration in the absence of epiplakin. The mechanism of cell proliferation stimulation by epiplakin knockdown is to be investigated.
Highlights
To investigate effects of knockdown of epiplakin gene expression on the homeostasis of cultured corneal epithelial cell line
In the present study we investigated behaviors, i.e., cell migration and proliferation, of epiplakinknockdowned cultured corneal epithelial cell line and examined the expression level of E-cadherin, keratin 6 and vimentin, both members of intermediate filament involved in cell migration [5], in the cells, decreased epiplakin expression does not solely explain the mechanism of cell migration acceleration in corneal epithelium
Present study was undertaken to uncover the roles of epiplakin in modulation of behaviors of cultured corneal epithelial cell line
Summary
To investigate effects of knockdown of epiplakin gene expression on the homeostasis of cultured corneal epithelial cell line. We previously reported acceleration of corneal epithelial wound healing in an epiplakin-null mouse. Human epiplakin is a 552-kDa protein that is expressed in various epithelial tissues, i.e., epidermis, esophagus, outer root sheath of hair follicles and mucous epithelial cells [1], [2]. Studies by using an epiplakin-null mouse line showed that lacking epiplakin accelerates migration of epidermal keratinocytes in mice in vivo and showed that this is the case in outgrowth of keratinocytes from explanted skin tissue in vitro, the exact mechanism of the phenomena is to be revealed [3]. We reported that corneal epithelium, a non-keratinizing stratified squamous epithelium, express epiplakin
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