Synergism between Jnk1 and Jnk2 is a sine qua non condition for hepatic protection against toxicity

Hepatocyte death, a feature of acute and chronic liver failure, is observable after acetoaminophen (APAP) poisoning in humans or LPS/GalN or CCl4-induced liver toxicity in mice. The activation of the c-Jun NH2 terminal kinase (JNK) intracellular signalling pathway during hepatocyte necrosis is a common molecular mechanism. In this context, the study of the shared functions of Jnk1 and Jnk2 in hepatocytes can be of utmost interest. Therefore, we generated mice with compound deletion of Jnk1 and Jnk2 in hepatocytes (JNKΔhepa) which were backcrossed several times to obtain the proper controls. All mice strains were…