Experimental & Molecular Medicine · 10 authors, 7 centres
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Using a mouse model of perforating corneal injury, this preclinical study shows that NFAT5 expression shifts from corneal fibroblasts to macrophages after injury and that loss of NFAT5, particularly in myeloid cells, accelerates corneal edema resorption through increased macrophage pinocytotic capacity.
NFAT5 expression was analyzed in naive and perforating corneal injury (PCI) mouse corneas. In uninjured corneas NFAT5 was expressed mainly in fibroblasts, while after PCI NFAT5 was highly upregulated in recruited corneal macrophages. NFAT5 deficiency did not alter central corneal thickness in steady state but led to accelerated resorption of corneal edema after PCI, as evidenced by significantly lower MCT in NFAT5-deficient versus control injured corneas. Conditional loss of NFAT5 in the myeloid lineage recapitulated this protective effect, and bone marrow-derived macrophages from myeloid-specific NFAT5 knockout mice showed significantly higher pinocytotic capacity. NFAT5 contributed to increased corneal Vegfc expression in injured tissues but this did not alter lymphatic vessel architecture. The authors propose that NFAT5 deficiency results in corneal macrophages with increased pinocytotic capacity, facilitating faster fluid removal.
