ArticleMolecular biology reports2025
CALR promotes corneal epithelial cell proliferation and migration through Wnt7a.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThe repair of corneal epithelial injury is essential to maintain the cornea integrity and transparency, and the molecular regulation mechanism is still unclear. CALR promotes wound healing through a variety of biological effects. Therefore, this study explored effect and mechanism of CALR on corneal epithelial wound healing.
methodsThe model of repairing corneal epithelium injury in mice was established, and corneal epithelial tissues were collected from the model group and the control group. oe-CALR or sh-Wnt7a was transfected into HCE-2[50.B1] cells by Lipofectamine 2000 to over-express CALR or knock down Wnt7a in vitro. CALR mRNA expression was detected by RT-qPCR. CCK-8, clone formation assay, cell senescence, flow cytometry, wound healing and Transwell migration assays were used to detect the changes in proliferation, cell senescence, cell cycle and cell migration after transfection. CALR, Wnt7a and β-catenin proteins expression were detected by Western blot. Interaction between CALR and Wnt7a was detected by Co-immunoprecipitation.
resultsCALR expression was increased in mice corneal epithelial injury repair, suggesting that CALR might play vital role in this process. CALR overexpression promoted HCE-2[50.B1] proliferation and migration, inhibited cell senescence of HCE-2[50.B1], and relieved S phase block and increased the number of HCE-2[50] cells in G0/G1 phase. Wnt7a and CALR proteins expression were respectively detected in the protein complexes co-precipitated by anti-CALR antibody and anti-Flag antibody. The interaction between CALR and Wnt7a could activate the downstream β-catenin signaling pathway. Wnt7a knockdown attenuated the effect of CALR overexpression on HCE-2[50.B1] cells proliferation, senescence and migration.
conclusionCALR promotes proliferation and migration, inhibited senescence of HCE-2[50.B1] cells by Wnt7a, thus promoting corneal epithelial wound healing. This study will provide a theoretical basis for mechanism of CALR in corneal injury repair, and provide a new target for corneal injury clinical treatment.
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