Moderate levels of ethanol induce expression of vascular endothelial growth factor and stimulate angiogenesis

Abstract

Alcohol abuse has a negative impact on human health; however, epidemiological studies show that moderate consumption of ethanol (EtOH) reduces the risk of coronary heart disease, sudden cardiac death, and ischemic stroke. The mechanisms for these reductions in cardiovascular disease are not well established. Using cultured coronary artery vascular smooth muscle cells, we found that moderate levels of EtOH (10 and 20 mM) caused dose-related increases in both vascular endothelial growth factor (VEGF) mRNA (Northern blot) expression (1.9- and 2.6-fold) and VEGF protein (ELISA) expression (19 and 68%) compared with control (P < 0.05). EtOH at 0.25 g. kg(-1). day(-1) (7 days) increased VEGF mRNA expression by 1.48-fold over control, and increased vessel length density from 3.9 +/- 0.7 (control) to 6.0 +/- 0.3 mm/mm(2) (P < 0.05) in chick chorioallantoic membrane (CAM). We conclude that moderate levels of ethanol can induce VEGF expression and stimulate angiogenesis in chick CAM. Therefore, the results provide a theoretical basis for speculating that the cardiovascular-protective effects of moderate alcohol consumption may be partly mediated through VEGF-induced angiogenesis.

Effects of a Single Dose of Ethanol on Survival Rate and Angiogenesis of Chick Embryo

“…EtOH has been reported to increase the angiogenesis using CAM assay (Gu, The results we represent indicate that moderate dose of EtOH does not affect vessels formation and heart development, which is in agreement with published study (Gu, Elam et al 2001). However, higher dose at 10% EtOH inhibit angiogenesis.…”

“…EtOH has been reported to affect the process of angiogenesis in CAM assay using chick embryo as model organism ( ) and yolk sac blood vessels system of early staged chick embryos (Karunamuni, Gu et al 2014). In an elegant study, it was reported that moderate dose of EtOH has positive effects on development of embryo particularly on vasculature of embryo (Gu, Elam et al 2001). These studies suggest that EtOH might cause an increase or decrease in angiogenesis, depending on EtOH dose and type of blood vessel system.…”

Modulation of Vascular Endothelial Growth Factor (VEGF) and Tissue Necrosis Factor Alpha (TNFα) by the Ethanol Stem Bark Extract of Boswellia dalzielli H Attenuates Ethanol Induced Gastric Ulcer in Albino Rats.

“…The result obtained is in accordance with previous studies that reported downregulation of enzymatic and non-enzymatic antioxidants. It was also reported that intragastric administration of absolute ethanol in rats increases the levels of VEGF, [22,23] TNF α, and MDA in gastric tissue homogenates. [24,25] Pretreatment of rats with graded doses of the ethanol stem bark extract of B. dalzielii H provided cytoprotection, signifi- cantly decreased (p<0.0001) gastric ulcer index, and ameliorated gastric mucosal injury by ethanol in a dose-dependent manner when compared to ethanol control.…”

“…It was argued that VEGF is elevated to dilute ethanol and other ulcerogenic products as a gastric protective mechanism. [22,31,23] VEGF prevents gastric mucosal injury by creating perivascular edema around subepithelial capillaries in the gastric mucosa to delay the absorption of toxic chemicals and minimize endothelial cell exposure to reduce or avert gastric injury. [32] Ranitidine is a reversible, competitive blocker of histamine at H 2 receptor on the parietal cells to decrease gastric acid secretion, reduce gastric juice volume, and reduce H+ concentration.…”

Spider angiomas in patients with liver cirrhosis: Role of vascular endothelial growth factor and basic fibroblast growth factor

“…Ethanol could induce expression of vascular endothelial growth factor and stimulate angiogenesis [26] . This may lead to the high prevalence of spider angiomas in alcoholic cirrhotic patients.…”