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Accelerated wound healing in tumor necrosis factor receptor p55‐deficient mice with reduced leukocyte infiltration

Accelerated wound healing in tumor necrosis factor receptor p55‐deficient mice with reduced... To clarify biological roles of tumor necrosis factor receptor p55 (TNF‐Rp55) ‐mediated signals in wound healing, skin excisions were prepared in BALB/c (WT) and TNF‐Rp55‐deficient (KO) mice. In WT mice, the wound area was reduced to 50% of the original area 6 days after injury, with angiogenesis and collagen accumulation. Histopathologically, reepithelialization rate was ~80% 6 days. Myeloperoxidase activity and macrophage recruitment were the most evident 1 and 6 days after injury, respectively. Gene expression of adhesion molecules, interleukin 1α(IL‐1α), IL‐1β, monocyte chemoattractant protein 1, macrophage inflammatory protein 1α(MIP‐1α), MIP‐2, transforming growth factor β1 (TGF‐β1) connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF), Flt‐1, and Flk‐1 was enhanced at the wound site. In KO mice, an enhancement in angiogenesis, collagen content, and reepithelialization was accelerated with the increased gene expression of TGF‐β1, CTGF, VEGF, Flt‐1, and Flk‐1 at the wound sites, resulting in accelerated wound healing compared with WT mice. In contrast, leukocyte infiltration, mRNA expression of adhesion molecules, and cytokines were significantly reduced in KO mice. These observations suggest that TNF‐Rp55‐mediated signals have some role in promoting leukocyte infiltration at the wound site and negatively affect wound healing, probably by reducing angiogenesis and collagen accumulation.—Mori, R., Kondo, T., Ohshima, T., Ishida, Y., Mukaida, N. Accelerated wound healing in tumor necrosis factor receptor p55‐deficient mice with reduced leukocyte infiltration. FASEB J. 16, 963–974 (2002) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The FASEB journal Wiley

Accelerated wound healing in tumor necrosis factor receptor p55‐deficient mice with reduced leukocyte infiltration

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References (70)

Publisher
Wiley
Copyright
© Federation of American Societies for Experimental Biology
ISSN
0892-6638
eISSN
1530-6860
DOI
10.1096/fj.01-0776com
Publisher site
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Abstract

To clarify biological roles of tumor necrosis factor receptor p55 (TNF‐Rp55) ‐mediated signals in wound healing, skin excisions were prepared in BALB/c (WT) and TNF‐Rp55‐deficient (KO) mice. In WT mice, the wound area was reduced to 50% of the original area 6 days after injury, with angiogenesis and collagen accumulation. Histopathologically, reepithelialization rate was ~80% 6 days. Myeloperoxidase activity and macrophage recruitment were the most evident 1 and 6 days after injury, respectively. Gene expression of adhesion molecules, interleukin 1α(IL‐1α), IL‐1β, monocyte chemoattractant protein 1, macrophage inflammatory protein 1α(MIP‐1α), MIP‐2, transforming growth factor β1 (TGF‐β1) connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF), Flt‐1, and Flk‐1 was enhanced at the wound site. In KO mice, an enhancement in angiogenesis, collagen content, and reepithelialization was accelerated with the increased gene expression of TGF‐β1, CTGF, VEGF, Flt‐1, and Flk‐1 at the wound sites, resulting in accelerated wound healing compared with WT mice. In contrast, leukocyte infiltration, mRNA expression of adhesion molecules, and cytokines were significantly reduced in KO mice. These observations suggest that TNF‐Rp55‐mediated signals have some role in promoting leukocyte infiltration at the wound site and negatively affect wound healing, probably by reducing angiogenesis and collagen accumulation.—Mori, R., Kondo, T., Ohshima, T., Ishida, Y., Mukaida, N. Accelerated wound healing in tumor necrosis factor receptor p55‐deficient mice with reduced leukocyte infiltration. FASEB J. 16, 963–974 (2002)

Journal

The FASEB journal – Wiley

Published: Jul 1, 2002

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