Cited by 194Wound Healing and TreatmentsTGF-β signaling in diseasesLiver physiology and pathology

Delayed Wound Healing in Immunodeficient TGF-β1 Knockout Mice

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Crowe, Maria J., Doetschman, Thomas, Greenhalgh, David G.·2000·Journal of Investigative Dermatology

Abstract

Previous studies showed that full-thickness wounds in transforming growth factor-beta1-deficient mice initially heal normally. Unfortunately, transforming growth factor-beta1 deficiency leads to a multifocal inflammatory disease affecting most organs of the body, which ultimately interferes with later stages of wound healing in these mice. As this inflammatory disease is eliminated in transforming growth factor-beta1-deficient mice lacking T and B cells (Tgfb1-/- Scid-/- mice), we hypothesized that wound repair in the latter would proceed normally, even at later stages of healing. Unexpectedly, Tgfb1-/- Scid-/- mice demonstrate a major delay of approximately 1 wk in each of the major phases of wound healing: inflammation, proliferation, and maturation. Immuno- deficient Scid-/- mice that have the wild-type Tgfb1 allele do not experience this delay in wound healing. One interpretation of these findings is that lymphocytes and transforming growth factor-beta1 affect compensatory pathways in wound healing. An alternative interpretation is that the delayed expression of Tgfb2 and Tgfb3 that occurs in the absence of transforming growth factor-beta1 results in the delayed wound healing, suggesting that transforming growth factor-beta2 and/or transforming growth factor-beta3 play important parts in wound healing.

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Crossref · 10.1046/j.1523-1747.2000.00010.x

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  • Bound and activated macrophages secrete chemoattractive factors that continue to recruit macrophages even after the initial implantation injury has resolved.

    “Bound and activated macrophages also secrete chemoattractive factors which continue to recruit macrophages even after the initial implantation injury has resolved (Crowe et al., 2000).”

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Authors
Crowe, M. J., Doetschman, T., & Greenhalgh, D. G.
Affiliations
  • Shriners Hospitals for Children - Cincinnati (US)
  • University of Cincinnati (US)
  • Shriners Hospitals for Children - Northern California (US)
Corresponding author
Doetschman, Thomas
Venue
Journal of Investigative Dermatology
Publisher
Elsevier BV
Published
2000-07
Volume
115
Issue
1
Pages
3-11
ISSN
0022-202X (ISSN-L)
OpenAlex
W2089230130
Cited by
194
References
58
Citations by year
2025: 3 · 2024: 9 · 2023: 6 · 2022: 7 · 2021: 9 · 2020: 12 · 2019: 3 · 2018: 10 · 2017: 7 · 2016: 8 · 2015: 5 · 2014: 5 · 2013: 10 · 2012: 12
FWCI
10.05
Type
journal article
Language
en
Open access
Locations
  • Journal of Investigative Dermatology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01gm050959-06)
  • National Institute of General Medical Sciences (R01 GM50959)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD026471, R01 HD26471)
Topics
  • Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
wound healing, TGF-β1, TGF-beta2, TGF-beta3, SCID mice, immunodeficiency, lymphocytes, inflammation, proliferation, wound maturation, compensatory pathways, full-thickness wounds
MeSH terms
Animals, Skin, Wound Healing, Wounds and Injuries, Gene Expression, Transforming Growth Factor beta, Mice, SCID, Apoptosis, Mice, Knockout, Mice

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