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Am J Physiol Gastrointest Liver Physiol 290: G1186-G1193, 2006. First published February 9, 2006; doi:10.1152/ajpgi.00282.2005
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HORMONES AND SIGNALING

Differential regulation of the JNK/AP-1 pathway by S-adenosylmethionine and methylthioadenosine in primary rat hepatocytes versus HuH7 hepatoma cells

Eduardo Ansorena,1 Carmen Berasain,2 María J. López Zabalza,1 Matías A. Ávila,2 Elena R. García-Trevijano,2 and María J. Iraburu1

1Departamento de Bioquímica y Biología Molecular, 2Area de Hepatología y Terapia Génica, Centro de Investigación Médica Aplicada, Universidad de Navarra, Navarra, Pamplona, Spain

Submitted 22 June 2005 ; accepted in final form 30 January 2006

S-adenosylmethionine (AdoMet) and 5'-methylthioadenosine (MTA) exert a protective action on apoptosis induced by okadaic acid in primary rat hepatocytes but not in human transformed HuH7 cells. In the present work, we analyzed the role played by the JNK/activator protein (AP)-1 pathway in this differential effect. Okadaic acid induced the phosphorylation of JNK and c-Jun and the binding activity of AP-1 in primary hepatocytes, and pretreatment with either AdoMet or MTA prevented those effects. In HuH7 cells, pretreatment with either AdoMet or MTA did not affect JNK and c-Jun activation or AP-1 binding induced by okadaic acid. In both cell types, p38 was activated by okadaic acid, but neither AdoMet nor MTA presented a significant effect on its activity. Therefore, the differential effect of both AdoMet and MTA on the JNK/AP-1 pathway could explain their antiapoptotic effect on primary hepatocytes and the lack of protection they show against okadaic acid-induced apoptosis in hepatoma cells.

okadaic acid; c-Jun; apoptosis; activator protein-1


Address for reprint requests and other correspondence: M. J. Iraburu, Departamento de Bioquímica y Biología Molecular, Universidad de Navarra, C/ Irunlarrea 1, 31008 Pamplona, Navarra, Spain (e-mail: miraburu{at}unav.es)






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