Abstract
Previous studies showed that full-thickness wounds in transforming growth factor-β1-deficient mice initially heal normally. Unfortunately, transforming growth factor-β1 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-β1-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. Immunodeficient 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-β1 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-β1 results in the delayed wound healing, suggesting that transforming growth factor-β2 and/or transforming growth factor-β3 play important parts in wound healing.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 3-11 |
| Number of pages | 9 |
| Journal | Journal of Investigative Dermatology |
| Volume | 115 |
| Issue number | 1 |
| DOIs | |
| State | Published - 2000 |
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Keywords
- Gene expression
- Knockout mice
- Skin injury
- Transforming growth factor-β isoforms
ASJC Scopus subject areas
- Dermatology
Cite this
Delayed wound healing in immunodeficient TGF-β1 knockout mice. / Crowe, Maria J.; Doetschman, Thomas; Greenhalgh, David G.
In: Journal of Investigative Dermatology, Vol. 115, No. 1, 2000, p. 3-11.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Delayed wound healing in immunodeficient TGF-β1 knockout mice
AU - Crowe, Maria J.
AU - Doetschman, Thomas
AU - Greenhalgh, David G
PY - 2000
Y1 - 2000
N2 - Previous studies showed that full-thickness wounds in transforming growth factor-β1-deficient mice initially heal normally. Unfortunately, transforming growth factor-β1 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-β1-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. Immunodeficient 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-β1 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-β1 results in the delayed wound healing, suggesting that transforming growth factor-β2 and/or transforming growth factor-β3 play important parts in wound healing.
AB - Previous studies showed that full-thickness wounds in transforming growth factor-β1-deficient mice initially heal normally. Unfortunately, transforming growth factor-β1 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-β1-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. Immunodeficient 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-β1 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-β1 results in the delayed wound healing, suggesting that transforming growth factor-β2 and/or transforming growth factor-β3 play important parts in wound healing.
KW - Gene expression
KW - Knockout mice
KW - Skin injury
KW - Transforming growth factor-β isoforms
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UR - http://www.scopus.com/inward/citedby.url?scp=0033926275&partnerID=8YFLogxK
U2 - 10.1046/j.1523-1747.2000.00010.x
DO - 10.1046/j.1523-1747.2000.00010.x
M3 - Article
C2 - 10886500
AN - SCOPUS:0033926275
VL - 115
SP - 3
EP - 11
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
SN - 0022-202X
IS - 1
ER -