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.
- Gene expression
- Knockout mice
- Skin injury
- Transforming growth factor-β isoforms
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