The loss of MCP-1 attenuates cutaneous ischemia-reperfusion injury in a mouse model of pressure ulcer

Yuki Saito, Minoru Hasegawa, Manabu Fujimoto, Takashi Matsushita, Mayuka Horikawa, Motoi Takenaka, Fumihide Ogawa, Junko Sugama, Douglas A. Steeber, Shinichi Sato, Kazuhiko Takehara

研究成果: Article査読

58 被引用数 (Scopus)

抄録

The formation of pressure ulcers is dependent on multiple factors including ischemia-reperfusion (IR). This study assessed the mechanism of a previously reported murine model of cutaneous IR injury. Three cycles of IR (days 1-3) by external application of two magnetic plates were performed to induce pressure ulcer formation. Increased infiltration of neutrophils and macrophages, and augmented expression of proinflammatory cytokines and inducible nitric oxide synthase (iNOS), were observed during IR cycles. In this model, monocyte chemoattractant protein-1 (MCP-1) was remarkably increased at day 1 in the skin followed by inflammatory cell infiltration. Therefore, IR cycles were performed in MCP-1-deficient (MCP-1-/-) mice to evaluate the role of this chemokine in pressure ulcer development. MCP-1-/- mice showed reduced macrophage infiltration and expression of tumor-necrosis factor-α (TNF)-α and iNOS during IR cycles leading to attenuated apoptosis and skin injury. Importantly, MCP-1 played a role in apoptosis and injury via inducing iNOS during the reperfusion rather than the ischemic period. These findings indicate that MCP-1 may be a critical factor for macrophage recruitment and subsequent skin inflammation and injury during IR cycles. We propose that this is a useful model for investigating the mechanism of pressure ulcer formation using various transgenic mice.

本文言語English
ページ(範囲)1838-1851
ページ数14
ジャーナルJournal of Investigative Dermatology
128
7
DOI
出版ステータスPublished - 07-2008
外部発表はい

All Science Journal Classification (ASJC) codes

  • 生化学
  • 分子生物学
  • 皮膚病学
  • 細胞生物学

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