TNF alpha-induced hepatocyte apoptosis is associated with alterations of the cell cycle and decreased stem loop binding protein.

Background: Inhibition of nuclear factor kappa B (NF kappa B) during liver regeneration induces hepatocyte apoptosis associated with normal DNA synthesis but decreased mitosis, suggesting that inhibition of NF kappa B impairs progression from S-phase through the G(2)/M phase of the cell cycle. Our aim was to determine if inhibition of NF kappa B alters cell cycle characteristics in hepatocytes treated with tumor necrosis factor alpha (TNF alpha).

Methods: Primary hepatocytes from BALB/c mice were infected with adenoviruses expressing luciferase (control; AdLuc) or the I kappa B super-repressor (AdI kappa B) and treated with or without TNF alpha (30 ng/ml).

Primary cirrhotic hepatocytes resist TGFbeta-induced apoptosis through a ROS-dependent mechanism.

Background/aims: The cirrhotic liver manifests dysregulated hepatocyte growth by poor regenerative capacity, formation of regenerative nodules, and malignant transformation to hepatocellular carcinoma. The purpose of this study was to determine if dysregulated hepatocyte growth occurs through deficient apoptosis.

Methods: Hepatocytes were isolated from normal and CCl(4)-treated mice and treated with TGFbeta, TNFalpha, and UV-C, known apoptotic agents.

Cirrhotic hepatocytes exhibit decreased TGFbeta growth inhibition associated with downregulated Smad protein expression.

TGFbeta controls hepatocyte growth through cell cycle arrest and apoptosis, and resistance to TGFbeta is a mechanism of malignant transformation. The aim of this study was to assess differences in TGFbeta-mediated growth inhibition in normal and cirrhotic hepatocytes. Cirrhosis was induced in mice and normal and cirrhotic hepatocytes were isolated by collagenase perfusion and treated with or without TGFbeta (5 ng/ml).

NFkappaB inhibition decreases hepatocyte proliferation but does not alter apoptosis in obstructive jaundice.

Introduction: Cholestasis activates nuclear factor kappa B (NFkappaB), which is involved in both hepatocyte proliferation and apoptosis, depending on the cellular microenvironment. We hypothesized that NFkappaB inhibition would decrease hepatocyte proliferation and potentiate hepatocyte apoptosis in a rat model of extrahepatic biliary obstruction.

Aim: To determine if NFkappaB inhibition concomitantly decreases hepatocyte proliferation and increases apoptosis in obstructive jaundice.

Transforming growth factor-beta1 induces hepatocyte apoptosis by a c-Jun independent mechanism.

Background: During hepatic regeneration, transforming growth factor (TGF)-beta1 messenger RNA increases after the initial cycle of DNA synthesis, and it may control hepatocyte growth by inducing apoptosis. TGF-beta1 also induces c-Jun, a potential proapoptotic transcription factor. We hypothesized that autocrine expression of activated TGF-beta1 (Ad5aTGF-beta1) would increase c-jun expression in rat liver and limit hepatic regeneration by inducing apoptosis.

Primary splenic lymphoma complicated by hematemesis and gastric erosion.

Gastrosplenic fistula resulting from erosion of a primary splenic lymphoma is a rare cause of massive upper gastrointestinal hemorrhage associated with benign peptic ulcer disease, gastric Crohn's disease, gastric adenocarcinoma, and primary gastric and splenic lymphomas. Upper intestinal hemorrhage can be successfully treated with splenic artery embolization, followed by splenectory and gastric resection.

Cholestasis induces murine hepatocyte apoptosis and DNA synthesis with preservation of the immediate-early gene response.

Background: Major hepatic resection in patients with unrelieved obstructive jaundice carries an increased risk of postoperative liver failure. We hypothesized that cholestasis induces hepatocyte apoptosis and impairs hepatic regeneration by inhibiting up-regulation of the known immediate-early response genes, nuclear factor kappa B (NF-kappaB) and activating protein-1 (AP-1). The aim of this study was to determine whether the immediate-early gene response in hepatic regeneration remains intact in extrahepatic cholestasis.