Accelerated wound healing in tumor necrosis factor receptor p55‐deficient mice with reduced leukocyte infiltration
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)
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Wound healing studies in TNF-Rp55−/− mice showed enhanced collagen accumulation with reduced leukocyte infiltration at wound sites.
“Wound healing studies in TNF-Rp55−/− mice showed in enhanced collagen accumulation with reduced leukocyte infiltration at wound sites.66”
From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [66]
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- Authors
- MORI, R., KONDO, T., OHSHIMA, T., ISHIDA, Y., & MUKAIDA, N.
- Affiliations
- Kanazawa University (JP)
- Division of Environmental Science Forensic and Social Environmental Medicine Graduate School of Medical Science
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2002-07
- Volume
- 16
- Issue
- 9
- Pages
- 963-974
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W1983346506
- Cited by
- 250
- References
- 63
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 2 · 2023: 7 · 2022: 8 · 2021: 4 · 2020: 11 · 2019: 9 · 2018: 10 · 2017: 12 · 2016: 14 · 2015: 16 · 2014: 15 · 2013: 10 · 2012: 16
- FWCI
- 12.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The FASEB Journal (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Keywords
- wound healing, leukocyte infiltration, angiogenesis, collagen deposition, re-epithelialization, macrophage recruitment, adhesion molecules, cytokines, TGF-β1, connective tissue growth factor, vascular endothelial growth factor, Flt-1, Flk-1, skin excision
- MeSH terms
- Animals, Cell Movement, Epidermis, Growth Substances, Hydroxyproline, Kinetics, Leukocytes, Male, Mice, Inbred BALB C, Peroxidase, RNA, Messenger, Skin, Skin Physiological Phenomena, Tumor Necrosis Factor-alpha, Wound Healing, Antigens, CD, Cell Adhesion Molecules, Cytokines, Receptors, Growth Factor, Receptors, Tumor Necrosis Factor, Mice, Knockout, Neovascularization, Physiologic, Receptor Protein-Tyrosine Kinases, Receptors, Vascular Endothelial Growth Factor, Receptors, Tumor Necrosis Factor, Type I, Receptors, Tumor Necrosis Factor, Type II, Mice
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