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mass spectrometry–based proteomics month download article/chapter sm-induced limbus injury tgf-β1/smad3 pathway colorado-anschutz medical campus mass spectrometry analysis human drug-metabolizing enzymes sulfur mustard toxicity writing—original draft preparation delayed/persistent structural damage barrier function-related genes rabbit limbal tissue mol cell proteomics sm-induced inflammatory references balali-mood full article pdf extracellular matrix proteins epithelial stem cells mesenchymal stem cells skeletal muscle cells acne-involved skin neutrophil-mediated inflammatory disease privacy choices/manage cookies antigen-presenting cells neera tewari-singh sulfur mustard oxidative stress inhibition mustard gas keratopathy multiple canonical pathways tissue injury dexamethasone treatment regimen significantly dysregulated proteins rajesh agarwal contributed significant proteins distributed corneal failure due recurrent corneal lesions persistent epithelial defects paraquat-triggered toxicity nuclear envelope rupture cgas-sting pathway corneal epithelial regeneration control limbal tissues drug/toxin metabolism article archives proteomics analysis corneal injuries delayed toxic effects rabbit ocular holds exclusive rights sm exposed

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         headline:Dexamethasone mitigates sulfur mustard-induced stem cell deficiency in vivo in rabbit limbal tissue by reducing inflammation and oxidative stress
         description:Sulfur mustard (SM) exposure induces ocular injury primarily to the cornea, limbus, and sclera. Although corneal injuries have been studied in detail, there is a dearth of literature on the effects of SM on limbus, particularly mechanisms underlying its compromised functioning, causing limbal stem cell deficiency (LSCD). LSCD causes impaired corneal repair leading to persistent epithelial defects, mustard gas keratopathy, and prolonged inflammation, resulting in total blindness in case of severe damage. Notably, dexamethasone (Dex) has been reported to treat SM-induced corneal injuries effectively; however, its efficacy for SM-induced limbus injury has not been studied. Hence, delayed/persistent structural damage (H&E and trichrome staining) and loss of LSCs [ΔNp63; immunofluorescence (IF)] in the limbus at day 28 post-SM exposure were assessed. Thereafter, in-depth proteomic analysis (LC–MS/MS) of SM exposed, Dex treated, and control limbal tissues (New Zealand white male rabbits) was performed. SM exposure significantly modulated the expression profile of 66 proteins, of which 62 were significantly reversed with Dex; thus, markedly inhibiting/hindering SM-induced limbal injury. Ingenuity Pathway Analysis predicted the primary involvement of (1) inflammation and immune response-associated pathways via dysregulation of defensin-5, eosinophil peroxidase, corticostatin-6, myeloperoxidase, and cathepsin C; and (2) drug/toxin metabolism and oxidative stress via GSTs, and ALDH1As modulations. IF analysis confirmed that Dex treatment significantly reversed SM-induced increases in human neutrophil peptides, defensin-5, and cathepsin C expression by 68%, 77%, and 90%, respectively. Thus, Dex markedly mitigated SM-induced limbal tissue injuries and prevented LSCD, via SM-induced inflammatory and oxidative stress inhibition, in our studies.
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      headline:Dexamethasone mitigates sulfur mustard-induced stem cell deficiency in vivo in rabbit limbal tissue by reducing inflammation and oxidative stress
      description:Sulfur mustard (SM) exposure induces ocular injury primarily to the cornea, limbus, and sclera. Although corneal injuries have been studied in detail, there is a dearth of literature on the effects of SM on limbus, particularly mechanisms underlying its compromised functioning, causing limbal stem cell deficiency (LSCD). LSCD causes impaired corneal repair leading to persistent epithelial defects, mustard gas keratopathy, and prolonged inflammation, resulting in total blindness in case of severe damage. Notably, dexamethasone (Dex) has been reported to treat SM-induced corneal injuries effectively; however, its efficacy for SM-induced limbus injury has not been studied. Hence, delayed/persistent structural damage (H&E and trichrome staining) and loss of LSCs [ΔNp63; immunofluorescence (IF)] in the limbus at day 28 post-SM exposure were assessed. Thereafter, in-depth proteomic analysis (LC–MS/MS) of SM exposed, Dex treated, and control limbal tissues (New Zealand white male rabbits) was performed. SM exposure significantly modulated the expression profile of 66 proteins, of which 62 were significantly reversed with Dex; thus, markedly inhibiting/hindering SM-induced limbal injury. Ingenuity Pathway Analysis predicted the primary involvement of (1) inflammation and immune response-associated pathways via dysregulation of defensin-5, eosinophil peroxidase, corticostatin-6, myeloperoxidase, and cathepsin C; and (2) drug/toxin metabolism and oxidative stress via GSTs, and ALDH1As modulations. IF analysis confirmed that Dex treatment significantly reversed SM-induced increases in human neutrophil peptides, defensin-5, and cathepsin C expression by 68%, 77%, and 90%, respectively. Thus, Dex markedly mitigated SM-induced limbal tissue injuries and prevented LSCD, via SM-induced inflammatory and oxidative stress inhibition, in our studies.
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         Sulfur mustard
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