Wnt7a can up-regulates cell adhesion related protein fibronectin expression and promotes cell proliferation in corneal epithelial cells

Abstract

Abstract Wingless-type MMTV integration site family member 7A (Wnt7a) is known as a ligand for members of the frizzled family receptors (FZDs) that functions in the canonical β-catenin signaling pathway and β-catenin independent pathways and plays an important role in embryonic development and homeostasis maintenance. Herein, we studied whether Wnt7a could promote the corneal epithelium proliferation and the specific mechanisms involved. In this study, expression level and distribution of Wnt7a protein in cornea slices was observed by immunohistochemistry and immunofluorescence assay. Human corneal epithelium cells (HCECs) were cultured in conditioned medium to observe the effect of Wnt7a on cell proliferation. Transcriptome sequencing was performed on the HCECs to analyze the possible role of Wnt7a. We found that, in natural states, Wnt7a protein was mainly concentrated in cells at the base of corneal limbus and a small amount was also distributed in the extracellular matrix of central cornea. After corneal epithelium injury, the expression of Wnt7a in central corneal epithelial cells was significantly increased. Cell wound scratch and CCK-8 assay proved that Wnt7a can promote HCECs proliferation in vitro. The transcriptome sequencing of HCECs cultured in conditional medium showed that Wnt7a could up regulate cell adhesion related genes such as fibronectin, which was verified by western blotting. These results showed that the expression pattern of Wnt7a changed after corneal epithelial injury, and Wnt7a directly participated in the repair after injury by upregulating fibronectin and promoting cell adhesion.