Identification of medical countermeasures for mustard-induced corneal blindness using RNA-seq analysis
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Introduction: Serious visual damage can arise from exposure to sulfur mustard (SM). Some eyes acquire permanent late ocular diseases that may cause corneal blindness, while some of the eyes demonstrate clinical resolution of the SM-injury. Improved treatment options may result from a better understanding of the pathogenic mechanisms that underlie the emergence of late pathology. Methods: The purpose of this study was to investigate the mRNA expression profiles of SM-induced damaged, undamaged, and naive corneas. RNA sequencing (RNA-seq) data (4 weeks post SM exposure) were used for differential expression (DE) analysis. The DE analysis of the damaged cornea group compared with the naive cornea group yielded a total of 5930 differentially expressed genes (upregulated:3196, downregulated:2734). The undamaged corneal group compared to the naive cornea group yielded 1884 differentially expressed genes (upregulated:1029, downregulated:855). When the damaged corneal group was compared with the undamaged corneal group, a total of 985 differentially expressed genes (upregulated: 308, downregulated: 677) were found. The log2(FC)[plus or minus] 2 and adjusted p[less than]0.05 were considered for screening of differentially expressed genes. The DE profiles were further subjected to pathway enrichment analysis. Results: The cell proliferation and differentiation pathways were studied to extract the top five upregulated genes (BTBD16, HEPACAM2, SLC15A3, L1CAM, MED17) common to both pathways. Furthermore, pathway analysis of cell migration, cell death, apoptotic processes, cell adhesion, extracellular matrix, and tumor necrosis factor production for the identification of novel genes and therapeutic targets is underway. Conclusion: This bioinformatic analysis shows promise for identifying novel therapeutic genes and pathways for keratopathy.
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This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License.