Hepatocyte Bcl-3 protects from death-receptor mediated apoptosis and subsequent acute liver failure.

ABSTRACT: Acute liver failure (ALF) is a rare entity but exhibits a high mortality. The mechanisms underlying ALF are not completely understood. The present study explored the role of the hepatic B cell leukemia-3 (Bcl-3), a transcriptional regulator of nuclear factor-kappa B (NF-κB), in two independent models of ALF. We employed a recently developed transgenic mouse model in a C57BL6/J background comparing wild-type (WT) and transgenic littermates with hepatocyte-specific overexpression of Bcl-3 (Bcl-3^Hep) in the ALF model of d-galactosamine (d-GalN) and lipopolysaccharide (LPS). Additionally, the apoptosis-inducing CD95 (FAS/APO-1)-ligand was explored. Bcl-3^Hep mice exhibited a significant protection from ALF with decreased serum transaminases, decreased activation of the apo

SUBMITTER: Gehrke N 

PROVIDER: S-EPMC9156769 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature