| First Author | Gore A | Year | 2025 |
| Journal | Ocul Surf | Volume | 37 |
| Pages | 247-259 | PubMed ID | 40287061 |
| Mgi Jnum | J:375236 | Mgi Id | MGI:8264670 |
| Doi | 10.1016/j.jtos.2025.04.007 | Citation | Gore A, et al. (2025) Use of a transgenic mouse model for in vivo monitoring of corneal pathologies following Sulfur Mustard Exposure. Ocul Surf 37:247-259 |
| abstractText | PURPOSE: The dynamic course of sulfur mustard (SM)-induced ocular insult involves an acute phase, which may progress to a chronic phase or a quiescent period, followed by late pathology. Visualizing pathological corneal changes in vivo could enhance understanding of this process and aid treatment development. METHODS: SM burn was induced in the right eyes of three transgenic mouse strains-expressing RFP under the VE-Cadherin promoter (blood vessels and hematopoietic cells), GFP under the keratin 15 promoter (limbal stem cells), and YFP under the Thy-1 promoter (mid-stromal nerve fibers, MSNFs)-by vapor exposure. Cell infiltration, neovascularization (NV), innervation loss, and stem cell (SC) depletion were monitored in vivo by stereomicroscopy for up to 8 weeks. Corneal whole-mounts were used to assess 360 degrees structures, infiltrating cells, and subbasal nerve plexus (SNP) loss. Histology included H&E, Masson-Trichrome, and periodic acid-Schiff staining. RESULTS: A 35-s exposure caused minor ocular insult with moderate SNP changes, corneal cell infiltration, and reversible SC loss, mostly resolving by 4 weeks. A 120-s exposure caused severe insult with NV, extensive MSNF and SNP loss, marked CD45(+) and Iba1(+) infiltration, and irreversible SC depletion. NV, stromal inflammation, edema, epithelial changes, and goblet cells were seen in histology and correlated with fluorescence imaging. CONCLUSIONS: This study demonstrates the utility of transgenic mice as powerful models for studying SM-induced ocular injury and for developing novel therapeutic strategies. |
