Ectodysplasin regulates corneal epithelial cell proliferation

Abstract

Purpose: Ectodysplasin (Eda) is a protein encoded by Eda gene. Mutation of this gene could cause X-linked Hypohidrotic Ectodermal Dysplasia (XLHED) disease in human. Ocular surface change in XLHED patients have been reported while the mechanism remains elusive. Our objective was to identify the effect of Eda protein on the corneal epithelium.

Methods: The ocular surface of Eda gene mutant mice (Tabby mice) were observed under slit lamp microscope. EGFR, EDAR and Ki67 expression in the corneal epithelium were performed by immunostaining, Western blot and quantitative real-time PCR assay. The cell counting kit-8 (CCK8) assay and scratch wound healing assay were performed to investigate the role of Eda on the migration and proliferation of human corneal epithelial cell line (HCE).

Results: H&E staining revealed thinner corneal epithelium in the early stage of Tabby mice, compared with the littermates. Ki67 positive cells decreased and EGFR expression was lower in the corneal epithelium of Tabby mice. Corneal epithelial wound healing delayed in Tabby mice, and the medium containing the Eda protein could accelerate the corneal epithelial cell wound healing in vitro. In HCE cell line, the Eda protein promotes the cell proliferation but not migration, EGFR expression in HCE cells was increased after Eda treatment.

Conclusions: Eda protein promotes corneal epithelial cell proliferation. Eda may be used in the treatment of corneal epithelial wounding.