Ethanol Inhibits Fibroblast Growth Factor–Induced Proliferation of Aortic Smooth Muscle Cells

Abstract

Objective-Epidemiological studies have demonstrated that moderate alcohol consumption reduces mortality associated with coronary artery disease. The protective effect is correlated with the amount of ethanol consumed but is unrelated to the form of alcoholic beverage. Adoption of a favorable lipoprotein profile accounts for about half of the protective action of alcohol, but the remaining causative factors remain conjectural. Fibroblast growth factors (FGFs) play important roles in mediating smooth muscle cell (SMC) proliferation and migration, which are key factors in the atherosclerotic process. In the present study, we examined the effect of ethanol on FGF-mediated SMC growth and signaling. Methods and Results-Pharmacologically relevant concentrations of ethanol inhibited the proliferation of a rat aortic SMC line (SV40LT-SMCs) in response to FGF1 and FGF2. Human aortic SMC growth was similarly inhibited by ethanol. Transition into the G 2 /M phase was specifically affected. FGF-mediated phosphorylation of p42/p44 mitogen-activated protein kinase (MAPK) c-Raf, MAP kinase kinase kinase, MEK1/2 MAP kinase, kinase, stress-activated protein kinase/c-Jun-NH 2 -terminal kinase, and p38 MAPK were variably reduced by ethanol. The inhibition of intracellular signaling by ethanol was correlated with inhibition of FGF receptor autophosphorylation. By contrast, neither epidermal growth factor receptor autophosphorylation nor epidermal growth factor-mediated p42/p44 MAPK activation was affected by ethanol. Conclusions-The

Unilateral right ductus with left aortic arch: an uncommon association

“…34 35 More recently it has been shown that alcohol inhibits fibroblast growth factor induced proliferation of aortic smooth muscle cells. 36 Together with the present findings, a strong body of evidence has accumulated to suggest a protective role of alcohol against vascular smooth muscle cell proliferation in atherosclerosis and restenosis after coronary interventions. A 25 year old woman was referred to the cardiac centre with a six month history of deteriorating cyanosis, dyspnoea, and exercise intolerance stable since early childhood.…”

The molecular mechanism of actinomycin D in preventing neointimal formation in rat carotid arteries after balloon injury

“…It is worth of mentioning that the level of phosphorylated-Erk 1/2 was up-regulated by actinomycin D in this study and was somewhat contradictory to the putative function of Erk as a critical signaling molecule leading to cell proliferation and survival [30,31]. However, one study showing that DNA damage can be initiated by Erk 1/2 phosphorylation may explain our present finding [32].…”

Biodegradable elastomeric scaffolds with basic fibroblast growth factor release

“…There may have been further activity that was undetectable at lower levels due to the variability associated with this type of assay, or alternatively, the lack of bioactivity after 3 weeks was due to bFGF denaturation in the scaffold over time although the amount of bFGF released during days 22-28 is comparable to that released during days 15-21. bFGF has been shown to induce the proliferation of endothelial cells, fibroblasts and smooth muscle cells. [48][49][50] For angiogenesis stimulation, heparin is often added to induce endothelial cell growth. [51,52] However, high concentrations of heparin inhibit the proliferation of smooth muscle cells.…”