RGD Reference Report - Ethanol inhibits fibroblast growth factor-induced proliferation of aortic smooth muscle cells. - Rat Genome Database

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Ethanol inhibits fibroblast growth factor-induced proliferation of aortic smooth muscle cells.

Authors: Ghiselli, Giancarlo  Chen, Jia  Kaou, Mohamad  Hallak, Hazam  Rubin, Raphael 
Citation: Ghiselli G, etal., Arterioscler Thromb Vasc Biol. 2003 Oct 1;23(10):1808-13. doi: 10.1161/01.ATV.0000090140.20291.CE. Epub 2003 Aug 7.
RGD ID: 155882535
Pubmed: PMID:12907464   (View Abstract at PubMed)
DOI: DOI:10.1161/01.ATV.0000090140.20291.CE   (Journal Full-text)


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 G2/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-NH2-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 findings identify the FGF receptor as an inhibitory target for ethanol, which could account in part for the inhibitory actions of ethanol on SMC proliferation observed in vivo.

Gene-Chemical Interaction Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
ethanol multiple interactionsISOFgfr2 (Rattus norvegicus)155882535; 155882535Ethanol inhibits the reaction [FGF2 protein increases phosphorylation of Fgfr2 protein in aortic smooth muscle cells]RGD 
ethanol multiple interactionsEXP 155882535Ethanol inhibits the reaction [FGF2 protein increases phosphorylation of Fgfr2 protein in aortic smooth muscle cells]RGD 

Objects Annotated

Genes (Rattus norvegicus)
Fgfr2  (fibroblast growth factor receptor 2)

Genes (Mus musculus)
Fgfr2  (fibroblast growth factor receptor 2)

Genes (Homo sapiens)
FGFR2  (fibroblast growth factor receptor 2)


Additional Information