Phosphotidylethanol mimics ethanol modulation of p42/44 mitogen-activated protein kinase signalling in hepatocytes.
Alcohol Alcohol
; 37(6): 534-9, 2002.
Article
em En
| MEDLINE
| ID: mdl-12414543
ABSTRACT
AIMS:
Although long-term exposure of hepatocytes to ethanol results in agonist-selective potentiation of p42/44 mitogen-activated protein kinase (MAPK) activation, mediators of this effect of ethanol are not known.METHODS:
We examined the role of phosphatidylethanol (PEth), a novel phospholipid formed exclusively in the presence of ethanol.RESULTS:
PEth accumulated in primary cultures of rat hepatocytes treated with ethanol. Exogenously added PEth potentiated angiotensin II-stimulated p42/44 MAPK similarly to that observed with ethanol treatment of cells for 24 h, a condition where PEth accumulates. PEth levels remained elevated 2 h after ethanol removal subsequent to a 24-h exposure, and the potentiating effects of ethanol were also present. PEth did not potentiate p42/44 MAPK activation by either epidermal growth factor or vasopressin, thus further mimicking the known agonist selectivity for this ethanol effect.CONCLUSIONS:
These results offer a novel role for PEth as a mediator in the ethanol modulation of p42/44 MAPK cascade in hepatocytes.
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Base de dados:
MEDLINE
Assunto principal:
Depressores do Sistema Nervoso Central
/
Glicerofosfolipídeos
/
Proteínas Quinases Ativadas por Mitógeno
/
Hepatócitos
/
Etanol
Limite:
Animals
Idioma:
En
Revista:
Alcohol Alcohol
Ano de publicação:
2002
Tipo de documento:
Article
País de afiliação:
Estados Unidos