Literature DB >> 17964119

Sulfur mustard downregulates iNOS expression to inhibit wound healing in a human keratinocyte model.

Hiroshi Ishida1, Radharaman Ray, Prabhati Ray.   

Abstract

BACKGROUND: Increased nitric oxide (NO) synthesized by inducible NO synthase (iNOS) is involved in inflammatory and pathological conditions. iNOS also regulates several biomarkers that accelerate normal wound healing. Effects of exposure to sulfur mustard (SM) on the skin include formation of blisters and slow-healing injuries. Promoting re-epithelialization is a challenging issue in the treatment of the delayed healing of SM-induced skin injuries.
OBJECTIVES: To clarify the role(s) of iNOS in wound healing and the effect of SM on iNOS expression in an in vitro wound assay to eventually develop therapies for SM skin injuries.
METHODS: A wound was created by scratching normal human epidermal keratinocytes grown in vitro. iNOS expression was monitored by Western blotting, fluorescence microscopy, and real-time RT-PCR. Wound healing was analyzed using digitalized image analysis software.
RESULTS: The level of iNOS peaked 24-48h after wounding. SM exposure strongly reduced iNOS protein and mRNA levels. Fluorescence microscopy revealed that induction of iNOS expression by wounding and inhibition of iNOS expression by SM occurred not only in the cells at the wound edge but also in cells in the surrounding area, suggesting that wounding may induce and SM may inhibit release of cytokines that stimulate iNOS expression. iNOS-specific small interfering RNAs caused a marked decrease of iNOS expression irrespective of wounding. Gene silencing also completely inhibited wound healing.
CONCLUSION: These results suggest that preventing SM-induced inhibition of iNOS may be a prospective strategy to promote wound healing in SM-exposed skin.

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Year:  2007        PMID: 17964119     DOI: 10.1016/j.jdermsci.2007.09.002

Source DB:  PubMed          Journal:  J Dermatol Sci        ISSN: 0923-1811            Impact factor:   4.563


  6 in total

1.  Sulfur mustard analog, 2-chloroethyl ethyl sulfide-induced skin injury involves DNA damage and induction of inflammatory mediators, in part via oxidative stress, in SKH-1 hairless mouse skin.

Authors:  Anil K Jain; Neera Tewari-Singh; Mallikarjuna Gu; Swetha Inturi; Carl W White; Rajesh Agarwal
Journal:  Toxicol Lett       Date:  2011-06-21       Impact factor: 4.372

2.  Time course pathogenesis of sulphur mustard-induced skin lesions in mouse model.

Authors:  Vinay Lomash; Sunil E Jadhav; Rajagopalan Vijayaraghavan; Satish C Pant
Journal:  Int Wound J       Date:  2012-06-04       Impact factor: 3.315

Review 3.  Mechanisms mediating the vesicant actions of sulfur mustard after cutaneous exposure.

Authors:  Michael P Shakarjian; Diane E Heck; Joshua P Gray; Patrick J Sinko; Marion K Gordon; Robert P Casillas; Ned D Heindel; Donald R Gerecke; Debra L Laskin; Jeffrey D Laskin
Journal:  Toxicol Sci       Date:  2009-10-15       Impact factor: 4.849

4.  Sulfur mustard induces an endoplasmic reticulum stress response in the mouse ear vesicant model.

Authors:  Yoke-Chen Chang; James D Wang; Kathy K Svoboda; Robert P Casillas; Jeffrey D Laskin; Marion K Gordon; Donald R Gerecke
Journal:  Toxicol Appl Pharmacol       Date:  2013-01-26       Impact factor: 4.219

5.  Nitric oxide synthase gene transfer overcomes the inhibition of wound healing by sulfur mustard in a human keratinocyte in vitro model.

Authors:  Hiroshi Ishida; Radharaman Ray; Jack Amnuaysirikul; Keiko Ishida; Prabhati Ray
Journal:  ISRN Toxicol       Date:  2012-11-14

6.  Early indicators of survival following exposure to mustard gas: Protective role of 25(OH)D.

Authors:  Lopa M Das; Amy M Binko; Zachary P Traylor; Lori R Duesler; Scott M Dynda; Sara Debanne; Kurt Q Lu
Journal:  Toxicol Lett       Date:  2016-03-02       Impact factor: 4.372

  6 in total

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