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Delayed Wound Healing in Immunodeficient TGF-β1 Knockout Mice
Open accessAbstract
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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“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).”
From Foreign Body Reaction to Implanted Biomaterials and Its Impact in Nerve Neuroprosthetics (2021) · cites this paper as Crowe et al., 2000
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Metadata
- 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
- ORCID
- Greenhalgh, David G.
- 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
- bronze
- doi.org
- Licence
- 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 › Surgery › 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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