Combined Activities of JNK1 and JNK2 in Hepatocytes Protect Against Toxic Liver Injury.

ABSTRACT:

Background & aims

c-Jun N-terminal kinase (JNK) 1 and JNK2 are expressed in hepatocytes and have overlapping and distinct functions. JNK proteins are activated via phosphorylation in response to acetaminophen- or carbon tetrachloride (CCl4)-induced liver damage; the level of activation correlates with the degree of injury. SP600125, a JNK inhibitor, has been reported to block acetaminophen-induced liver injury. We investigated the role of JNK in drug-induced liver injury (DILI) in liver tissue from patients and in mice with genetic deletion of JNK in hepatocytes.

Methods

We studied liver sections from patients with DILI (due to acetaminophen, phenprocoumon, nonsteroidal anti-inflammatory drugs, or autoimmune hepatitis) or patients without acute liver failure (controls) colle

SUBMITTER: Cubero FJ 

PROVIDER: S-EPMC5285516 | biostudies-literature | 2016 Apr

REPOSITORIES: biostudies-literature