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

D Meisse, M Van de Casteele, C Beauloye… - FEBS …, 2002 - Wiley Online Library
D Meisse, M Van de Casteele, C Beauloye, I Hainault, BA Kefas, MH Rider, F Foufelle
FEBS letters, 2002Wiley Online Library
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 …
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.
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