Decreased proteasomal function increases oxidative stress in the early stage of pressure ulcer

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  • Murata Eri
    Dept. of Nursing, Faculty of Medicine & Graduate Sch. of Medicine, Yamagata Univ.
  • Yoshida Takuma
    Dept. of pathology, Faculty of Medicine & Graduate Sch. of Medicine, Hokkaido Univ.
  • Yamamoto Saaki
    Dept. of pathology, Faculty of Medicine & Graduate Sch. of Medicine, Hokkaido Univ.
  • Ishizu Akihiro
    Dept. of Medical Laboratory Science, Faculty of Health Sci., Hokkaido Univ.
  • Tomaru Utano
    Dept. of pathology, Faculty of Medicine & Graduate Sch. of Medicine, Hokkaido Univ.

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Other Title
  • プロテアソーム機能低下が早期の褥瘡形成に与える影響

Abstract

<p>&lt;Background and Objective&gt; Decubitus ulcer is a tissue necrosis caused by skin pressure and circulation disturbance, and recent reports indicate that increased oxidative stress due to ischemia-reperfusion (IRI) contributes to the pathogenesis. Proteasome, an intracellular proteolytic enzyme complex, plays an important role in the oxidative stress response. In this study, we investigated the effect of proteasomal function on pressure ulcers (PUs).</p><p>&lt;Methods&gt; Using mice with impaired proteasome function, we analyzed changes in PUs and oxidative stress and expression of oxidative stress-related molecules after skin IRI. We also examined the effect of free radical scavenger (EDA) treatment on PUs. Using mouse skin fibroblasts, we examined the changes in cellular oxidative stress induced by proteasome inhibitors and hypoxia/reoxygenation.</p><p>&lt;Results and Discussion&gt; We found that proteasomal dysfunction exacerbated PUs and increased oxidative stress due to redox imbalance. In addition, the treatment of EDA reduced tissue injury. Proteasomal function declines with age and has been noted to play a role in the pathogenesis of aging and aging-related diseases. In the elderly, it is possible that the decreased proteasomal function induces excessive oxidative stress due to IRI, which increases the risk of severe PUs.</p>

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