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1 Burn and Shock Trauma Institute, Loyola University Medical Center, Maywood, IL, USA; Alcohol Research Program, Loyola University Medical Center, Maywood, IL, USA; Division of Molecular and Cellular Biochemistry, Loyola University Medical Center, Maywood, IL, USA
2 Burn and Shock Trauma Institute, Loyola University Medical Center, Maywood, IL, USA; Department of Microbiology and Immunology, Loyola University Medical Center, Maywood, IL, USA
3 Burn and Shock Trauma Institute, Loyola University Medical Center, Maywood, IL, USA
4 Burn and Shock Trauma Institute, Loyola University Medical Center, Maywood, IL, USA; Alcohol Research Program, Loyola University Medical Center, Maywood, IL, USA; Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Medical Center, Maywood, IL, USA
5 Burn and Shock Trauma Institute, Loyola University Medical Center, Maywood, IL, USA; Alcohol Research Program, Loyola University Medical Center, Maywood, IL, USA; Department of Surgery, Loyola University Medical Center, Maywood, IL, USA
* To whom correspondence should be addressed. E-mail: Ldipiet{at}Lumc.edu.
Acute ethanol exposure represents an increased risk factor for morbidity and mortality associated with surgical or traumatic injury. Despite clinical observations suggesting that ethanol exposure prior to injury alters tissue repair processes, little direct evidence about the mechanism by which ethanol affects the wound healing process is available. In this study, excisional wounds from female BALB/c mice with or without circulating ethanol levels of 100 mg/dl were used to assess wound closure, angiogenesis, and collagen content. Ethanol exposure resulted in a significant but transient delay in wound closure at day 2 post-wounding (28 ± 4% vs. 17 ± 1%). In addition, total collagen content was significantly reduced by up to 37% in wounds from ethanol treated mice compared to controls. The most significant effect of ethanol exposure on wounds was on vascularity, as angiogenesis was reduced by up to 61% in wounds from ethanol treated mice. The reduction in vessel density occurred despite near-normal levels of proangiogenic factors, VEGF and FGF-2, suggesting a direct effect of ethanol exposure on endothelial cell (EC) function. Further evidence for a direct effect was observed in an in vitro angiogenesis assay, as the exposure of EC to ethanol reduced angiogenic responsiveness to just 8.33% of control in a cord-forming assay. These studies provide novel information regarding the effect of a single dose of ethanol on multiple parameters of the wound healing process in vivo and suggest a potential mechanism by which ethanol impairs healing following traumatic injury.
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