Delayed wound healing in immunodeficient TGF-β1 knockout mice

Maria J. Crowe, Thomas Doetschman, David G Greenhalgh

Research output: Contribution to journalArticle

127 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)3-11
Number of pages9
JournalJournal of Investigative Dermatology
Volume115
Issue number1
DOIs
StatePublished - 2000

Fingerprint

Transforming Growth Factors
Knockout Mice
Wound Healing
Lymphocytes
Wounds and Injuries
Repair
B-Lymphocytes
Alleles
Cells
Inflammation
T-Lymphocytes

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 journalArticle

Crowe, Maria J. ; Doetschman, Thomas ; Greenhalgh, David G. / Delayed wound healing in immunodeficient TGF-β1 knockout mice. In: Journal of Investigative Dermatology. 2000 ; Vol. 115, No. 1. pp. 3-11.
@article{9ed2422c67084acabdeb61a0af632b95,
title = "Delayed wound healing in immunodeficient TGF-β1 knockout mice",
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.",
keywords = "Gene expression, Knockout mice, Skin injury, Transforming growth factor-β isoforms",
author = "Crowe, {Maria J.} and Thomas Doetschman and Greenhalgh, {David G}",
year = "2000",
doi = "10.1046/j.1523-1747.2000.00010.x",
language = "English (US)",
volume = "115",
pages = "3--11",
journal = "Journal of Investigative Dermatology",
issn = "0022-202X",
publisher = "Nature Publishing Group",
number = "1",

}

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

UR - http://www.scopus.com/inward/record.url?scp=0033926275&partnerID=8YFLogxK

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 -