Acute ethanol increases angiogenic growth factor gene expression in rat skeletal muscle

Gavin, Timothy P.; Wagner, Peter D.

doi:10.1152/japplphysiol.00929.2001

Cited by 17 publications

(10 citation statements)

References 41 publications

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“…Thus it seems likely that the effect of ethanol on wound angiogenesis is more complex than a simple reduction in the proangiogenic stimulus. Interestingly, ethanol exposure has also been shown to increase both FGF-2 and VEGF levels in exercised skeletal muscle (14).…”

Section: Discussionmentioning

confidence: 99%

Acute ethanol exposure impairs angiogenesis and the proliferative phase of wound healing

Radek

Matthies

Burns

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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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 before 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 postwounding (28 ± 4% vs. 17 ± 1%). In addition, total collagen content was significantly reduced by up to 37% in wounds from ethanol-treated mice compared with controls. The most significant effect of ethanol exposure on wounds was on vascularity because 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 function. Further evidence for a direct effect was observed in an in vitro angiogenesis assay because the exposure of endothelial cells 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 after traumatic injury.

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Section: Discussionmentioning

confidence: 99%

Acute ethanol exposure impairs angiogenesis and the proliferative phase of wound healing

Radek

Matthies

Burns

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…Ethanol is known to induce many pro-angiogenic growth factors and receptors including VEGF, basic fibroblast growth factor (bFGF), transforming growth factor β (TGF-β), VEGF receptor 1 and VEGF receptor 2 resulting in angiogenesis not mediated by immune inflammatory mechanisms. Therefore, reducing the concentration of ethanol creates a more accurate representation of the role of VEGF-A in colitis [19]. Although the concentration of ethanol was lower in our model it was sufficient to disrupt the epithelial barrier and allow TNBS to initiate immune mediated inflammation and significant elevation of disease activity.…”

Section: Discussionmentioning

confidence: 99%

VEGF-A isoform modulation in an preclinical TNBS model of ulcerative colitis: protective effects of a VEGF164b therapy

et al. 2013

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BackgroundUlcerative colitis (UC) is the most common form of inflammatory bowel disease in the USA. A key component of UC is the increase in inflammatory angiogenesis of the colon during active disease. This increase is driven to a great extent by the over expression of VEGF-A. Recently, VEGF165b (VEGF164b in mouse), an anti-angiogenic form of VEGF-A was described and its regulation was determined to be disturbed in many pathologies such as cancer and pre-eclampsia.ResultsThe aims of this study were to examine the role of this inhibitory VEGF by expressing this molecule in a model of intestinal inflammation, and to evaluate its expression as a potential new therapeutic approach for treating UC. A modified model of TNBS colitis was used to determine the effects of rVEGF164b expression on colon inflammation. Expansion of the vascular system was assessed by immunhistochemical methods and macro- and microscopic measurements of inflammation in the colon were measured. Leukocyte invasion of the tissue was measured by myeloperoxidase assay and identification and counting of lymphoid follicles. Both angio- and lymphangiogenesis were reduced by expression of rVEGF164b, which correlated with reduction in both gross and microscopic inflammatory scores. Leukocyte invasion of the tissue was also reduced by rVEGF164b expression.ConclusionsThis is the first report using an endogenous inhibitory VEGF-A isoform for therapy in a model of experimental colitis. Inhibitory VEGF molecules play an important role in maintenance of gut homeostasis and may be dysregulated in UC. The results of this study suggest that restoration of rVEGF164b expression has anti-inflammatory activity in a TNBS model and warrants further examination as a possible therapeutic for UC.

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“…On the other hand, several groups report a stimulatory effect of ethanol on angiogenesis (particularly in relation to tumorigenesis) in a variety of in vivo and in vitro models [73,90,91,92,93,94]. The mechanisms involved included ethanol stimulation of angiogenic growth factors such as vascular endothelial growth factor (VEGF) [90,92], basic fibroblast growth factor (bFGF) [92,93], and transforming growth factor beta (TGFβ)1 [93], while Qian et al provided evidence of a signaling pathway linking ethanol-induced changes in cell division control protein 42 homolog (Cdc42), H 2 O 2 , actin filaments and cell motility to in vitro angiogenesis [95]. Endothelial cell migration and proliferation are central to the process of new blood vessel formation and a biphasic effect of ethanol, whereby low dose ethanol (1–30 mM) stimulates and higher dose ethanol (30–100 mM) inhibits EC proliferation and migration has also been reported [53,96].…”

Section: Ethanol and Endothelial Proliferation Migration And Angimentioning

confidence: 99%

Alcohol and Cardiovascular Disease—Modulation of Vascular Cell Function

Cahill

Redmond

2012

Nutrients

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Alcohol is a commonly used drug worldwide. Epidemiological studies have identified alcohol consumption as a factor that may either positively or negatively influence many diseases including cardiovascular disease, certain cancers and dementia. Often there seems to be a differential effect of various drinking patterns, with frequent moderate consumption of alcohol being salutary and binge drinking or chronic abuse being deleterious to one’s health. A better understanding of the cellular and molecular mechanisms mediating the many effects of alcohol consumption is beginning to emerge, as well as a clearer picture as to whether these effects are due to the direct actions of alcohol itself, or caused in part by its metabolites, e.g., acetaldehyde, or by incidental components present in the alcoholic beverage (e.g., polyphenols in red wine). This review will discuss evidence to date as to how alcohol (ethanol) might affect atherosclerosis that underlies cardiovascular and cerebrovascular disease, and the putative mechanisms involved, focusing on vascular endothelial and smooth muscle cell effects.

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Acute ethanol increases angiogenic growth factor gene expression in rat skeletal muscle

Abstract: . Acute ethanol increases angiogenic growth factor gene expression in rat skeletal muscle.

Cited by 17 publications

References 41 publications

Acute ethanol exposure impairs angiogenesis and the proliferative phase of wound healing

Acute ethanol exposure impairs angiogenesis and the proliferative phase of wound healing

VEGF-A isoform modulation in an preclinical TNBS model of ulcerative colitis: protective effects of a VEGF164b therapy

Alcohol and Cardiovascular Disease—Modulation of Vascular Cell Function

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