Abstract
The epidermal growth factor receptor (EGFR) has been implicated in the regulation of wound healing. In order to directly evaluate the role of endogenous EGFR in cutaneous incisional wound healing, we examined EGFR null- and wild-type skin after injury. By 5 d after wounding, re-epithelialization was complete in all EGFR wild-type wounds, but in only 40% of EGFR null wounds. Delayed wound closure in EGFR null skin was accompanied by an increase in edema, longer lasting and more prominent eschar, and increased distance between apposing wound edges. EGFR altered neutrophil and mast cell infiltration, and enhanced angiogenesis. EGFR enhanced epithelial proliferation during the first 3 d following injury, although proliferation was greater in EGFR null wounds at 5 d. Although migration was decreased in EGFR null keratinocytes cultured with standard medium or in medium supplemented with transforming growth factor-α when compared with controls, the addition of the wound-associated motogen keratinocyte growth factor eliminated the differences between genotypes. Epithelial migration into the wound was decreased in EGFR null skin, suggesting that both EGFR-dependent and -independent mechanisms regulate migration during wound healing. These data demonstrate that EGFR regulates multiple facets of cutaneous wound healing, including inflammation, wound contraction, proliferation, migration, and angiogenesis.
| Original language | English |
|---|---|
| Pages (from-to) | 982-989 |
| Number of pages | 8 |
| Journal | Journal of Investigative Dermatology |
| Volume | 123 |
| Issue number | 5 |
| DOIs | |
| State | Published - Nov 2004 |
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All Science Journal Classification (ASJC) codes
- Dermatology
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EGFR enhances early healing after cutaneous incisional wounding. / Repertinger, Susan K.; Campagnaro, Erica; Fuhrman, Jill; El-Abaseri, Taghrid; Yuspa, Stuart H.; Hansen, Laura A.
In: Journal of Investigative Dermatology, Vol. 123, No. 5, 11.2004, p. 982-989.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - EGFR enhances early healing after cutaneous incisional wounding
AU - Repertinger, Susan K.
AU - Campagnaro, Erica
AU - Fuhrman, Jill
AU - El-Abaseri, Taghrid
AU - Yuspa, Stuart H.
AU - Hansen, Laura A.
PY - 2004/11
Y1 - 2004/11
N2 - The epidermal growth factor receptor (EGFR) has been implicated in the regulation of wound healing. In order to directly evaluate the role of endogenous EGFR in cutaneous incisional wound healing, we examined EGFR null- and wild-type skin after injury. By 5 d after wounding, re-epithelialization was complete in all EGFR wild-type wounds, but in only 40% of EGFR null wounds. Delayed wound closure in EGFR null skin was accompanied by an increase in edema, longer lasting and more prominent eschar, and increased distance between apposing wound edges. EGFR altered neutrophil and mast cell infiltration, and enhanced angiogenesis. EGFR enhanced epithelial proliferation during the first 3 d following injury, although proliferation was greater in EGFR null wounds at 5 d. Although migration was decreased in EGFR null keratinocytes cultured with standard medium or in medium supplemented with transforming growth factor-α when compared with controls, the addition of the wound-associated motogen keratinocyte growth factor eliminated the differences between genotypes. Epithelial migration into the wound was decreased in EGFR null skin, suggesting that both EGFR-dependent and -independent mechanisms regulate migration during wound healing. These data demonstrate that EGFR regulates multiple facets of cutaneous wound healing, including inflammation, wound contraction, proliferation, migration, and angiogenesis.
AB - The epidermal growth factor receptor (EGFR) has been implicated in the regulation of wound healing. In order to directly evaluate the role of endogenous EGFR in cutaneous incisional wound healing, we examined EGFR null- and wild-type skin after injury. By 5 d after wounding, re-epithelialization was complete in all EGFR wild-type wounds, but in only 40% of EGFR null wounds. Delayed wound closure in EGFR null skin was accompanied by an increase in edema, longer lasting and more prominent eschar, and increased distance between apposing wound edges. EGFR altered neutrophil and mast cell infiltration, and enhanced angiogenesis. EGFR enhanced epithelial proliferation during the first 3 d following injury, although proliferation was greater in EGFR null wounds at 5 d. Although migration was decreased in EGFR null keratinocytes cultured with standard medium or in medium supplemented with transforming growth factor-α when compared with controls, the addition of the wound-associated motogen keratinocyte growth factor eliminated the differences between genotypes. Epithelial migration into the wound was decreased in EGFR null skin, suggesting that both EGFR-dependent and -independent mechanisms regulate migration during wound healing. These data demonstrate that EGFR regulates multiple facets of cutaneous wound healing, including inflammation, wound contraction, proliferation, migration, and angiogenesis.
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U2 - 10.1111/j.0022-202X.2004.23478.x
DO - 10.1111/j.0022-202X.2004.23478.x
M3 - Article
C2 - 15482488
AN - SCOPUS:6344270007
VL - 123
SP - 982
EP - 989
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
SN - 0022-202X
IS - 5
ER -