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Sustained activation of AMP-activated protein kinase induces c-Jun N-terminal kinase activation and apoptosis in liver cells

par Meisse, Delphine;Van De Casteele, Christine ;Beauloye, Christophe;Hainault, Isabelle;Kefas, Benjamin Ate;Rider, Mark H.;Foufelle, Fabienne;Hue, Louis
Référence FEBS letters, 526, 1-3, page (38-42)
Publication Publié, 2002-08

Article révisé par les pairs

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Résumé :

The aim of this work was to study the effect of a sustained activation of AMP-activated protein kinase (AMPK) on liver cell survival. AMPK activation was achieved by incubating FTO2B cells with AICA-riboside, which is transformed into ZMP, an AMP analogue, or by adenoviral transfection of hepatocytes with a constitutively active form of AMPK. Prolonged AMPK activation triggered apoptosis and activated c-Jun N-terminal kinase (JNK) and caspase-3. Experiments with iodotubercidin, dicoumarol and z-VAD-fmk, which inhibited AMPK, JNK and caspase activation, respectively, supported the notion that prolonged AMPK activation in liver cells induces apoptosis through an activation pathway that involves JNK and caspase-3. © 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.