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Impaired skin barrier function caused by reactive oxygen species in mice with colonic tumours.

Abstract

Purpose:

We have previously reported that skin barrier function is disrupted in mice with colonic tumours induced by azoxymethane (AOM) and dextran sodium sulphate (DSS). We postulated that the impaired skin barrier function was associated with reactive oxygen species derived from gp91phox. In this study, we investigated the mechanisms underlying the impaired skin barrier function using gp91phox-/- mice. Materials and methods: We induced colonic tumorigenesis in C57BL/6j mice by AOM + DSS administration and evaluated the influence of reactive oxygen species on skin barrier function by using the hydroxyl radical scavenger N-acetyl-l-cysteine (NAC) or gp91phox-/- mice. Damage to the colon and skin following treatment with AOM + DSS was monitored using protein analysis methods and by detection of inflammatory mediators in the plasma.

Results:

NAC could not prevent the increase in transepidermal water loss (TEWL) and decrease in skin hydration level caused by AOM + DSS in gp91phox+/+ mice. However, gp91phox-/- mice showed no change in TEWL and skin hydration level. The dermal expression levels of nucleotide-binding domain, leucine-rich containing family, pyrin-domain containing 3 (NLRP3), and caspase-1 were reduced in gp91phox-/- mice. Moreover, the plasma concentrations of interleukin-18 and thymic stromal lymphopoietin (TSLP) were lower in gp91phox-/- mice than those in gp91phox+/+ mice. Inhibition of hydrogen peroxide production from superoxide anions in the gp91phox-/- status prevented the increased TEWL and decreased skin hydration level noted with degradation of NLRP3 and caspase-1.

Conclusions:

Superoxide anions may play an important role in the onset of the impaired skin barrier function in mice with colonic tumours.

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  • Authors+Show Affiliations

    ,

    a Division of Clinical Drug Informatics, School of Pharmacy , Kindai University , Osaka , Japan.

    ,

    b Faculty of Pharmaceutical Sciences , Suzuka University of Medical Science , Mie , Japan.

    b Faculty of Pharmaceutical Sciences , Suzuka University of Medical Science , Mie , Japan.

    Source

    Cutaneous and ocular toxicology : 2019 Jun 12 pg 1-7

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    31137980

    Citation

    Yokoyama, Satoshi, et al. "Impaired Skin Barrier Function Caused By Reactive Oxygen Species in Mice With Colonic Tumours." Cutaneous and Ocular Toxicology, 2019, pp. 1-7.
    Yokoyama S, Hiramoto K, Yamate Y. Impaired skin barrier function caused by reactive oxygen species in mice with colonic tumours. Cutan Ocul Toxicol. 2019.
    Yokoyama, S., Hiramoto, K., & Yamate, Y. (2019). Impaired skin barrier function caused by reactive oxygen species in mice with colonic tumours. Cutaneous and Ocular Toxicology, pp. 1-7. doi:10.1080/15569527.2019.1622559.
    Yokoyama S, Hiramoto K, Yamate Y. Impaired Skin Barrier Function Caused By Reactive Oxygen Species in Mice With Colonic Tumours. Cutan Ocul Toxicol. 2019 Jun 12;1-7. PubMed PMID: 31137980.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Impaired skin barrier function caused by reactive oxygen species in mice with colonic tumours. AU - Yokoyama,Satoshi, AU - Hiramoto,Keiichi, AU - Yamate,Yurika, Y1 - 2019/06/12/ PY - 2019/5/30/pubmed PY - 2019/5/30/medline PY - 2019/5/30/entrez KW - Gp91phox KW - NLRP3 KW - ROS KW - Skin barrier KW - TSLP KW - colonic tumours KW - superoxide anion SP - 1 EP - 7 JF - Cutaneous and ocular toxicology JO - Cutan Ocul Toxicol N2 - Purpose: We have previously reported that skin barrier function is disrupted in mice with colonic tumours induced by azoxymethane (AOM) and dextran sodium sulphate (DSS). We postulated that the impaired skin barrier function was associated with reactive oxygen species derived from gp91phox. In this study, we investigated the mechanisms underlying the impaired skin barrier function using gp91phox-/- mice. Materials and methods: We induced colonic tumorigenesis in C57BL/6j mice by AOM + DSS administration and evaluated the influence of reactive oxygen species on skin barrier function by using the hydroxyl radical scavenger N-acetyl-l-cysteine (NAC) or gp91phox-/- mice. Damage to the colon and skin following treatment with AOM + DSS was monitored using protein analysis methods and by detection of inflammatory mediators in the plasma. Results: NAC could not prevent the increase in transepidermal water loss (TEWL) and decrease in skin hydration level caused by AOM + DSS in gp91phox+/+ mice. However, gp91phox-/- mice showed no change in TEWL and skin hydration level. The dermal expression levels of nucleotide-binding domain, leucine-rich containing family, pyrin-domain containing 3 (NLRP3), and caspase-1 were reduced in gp91phox-/- mice. Moreover, the plasma concentrations of interleukin-18 and thymic stromal lymphopoietin (TSLP) were lower in gp91phox-/- mice than those in gp91phox+/+ mice. Inhibition of hydrogen peroxide production from superoxide anions in the gp91phox-/- status prevented the increased TEWL and decreased skin hydration level noted with degradation of NLRP3 and caspase-1. Conclusions: Superoxide anions may play an important role in the onset of the impaired skin barrier function in mice with colonic tumours. SN - 1556-9535 UR - https://www.unboundmedicine.com/medline/citation/31137980/Impaired_skin_barrier_function_caused_by_reactive_oxygen_species_in_mice_with_colonic_tumours L2 - http://www.tandfonline.com/doi/full/10.1080/15569527.2019.1622559 DB - PRIME DP - Unbound Medicine ER -