Abstract
Purpose :
A robust nerve regenerative response following corneal injury requires the coordinated expression of neurotrophic signaling molecules within the local environment. Galectin-3 is a carbohydrate-binding lectin overproduced in the cornea under various pathological conditions. The aim of this study was to evaluate whether galectin-3 affects the expression of neurotrophic factors in human corneal epithelial cells and fibroblasts.
Methods :
Human cadaveric corneas were obtained from Lions VisionGift. Primary corneal epithelial cells and fibroblasts were cultured and expanded in vitro. RNA and conditioned media were collected from cell cultures treated with recombinant human galectin-3 (rhGal-3). The analysis of genes related to neuronal processes was carried out using a human Neurotrophin and Receptors PCR array and qPCR. Protein secretion was measured by ELISA.
Results :
The expression of 5 genes, out of 84 genes present on the PCR array, was upregulated more than 2-fold in cells treated with rhGal-3. BDNF and FRS3, which help support neuron survival and growth, were upregulated in corneal epithelial cells. In fibroblasts, rhGal-3 increased the expression of the neuroprotective factors NRG4 and TGFA. Interestingly, addition of rhGal-3 to cultures of human fibroblasts increased the expression of IL6, a cytokine previously found to inhibit nerve regeneration in sterile and viral-induced corneal injury. The upregulation of IL6 was further confirmed by qPCR and ELISA.
Conclusions :
The present study indicates that galectin-3 exhibits neurotrophic effects in the human cornea and suggest a role for this lectin in modulating the balance between neuroprotective and proinflammatory neurotoxic mediators.
This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.