4-Hydroxynonenal-induced apoptosis in rat hepatic stellate cells: mechanistic approach.

Background And Aim: Although lipid peroxidation products act as apoptotic signals for several cell types, including hepatic stellate cells, the underlying mechanisms are not well understood. In this study we determined if: (i) 4-hydroxy-2,3-nonenal (HNE) induces apoptosis in two rat stellate cell lines, HSC-T6 and CFSC-2G; and (ii) if apoptosis is regulated at the transcriptional and/or translational level.

Methods: HSC-T6 and CFSC-2G cells were treated with HNE and total RNA and protein extracted.

Group V sPLA2 hydrolysis of low-density lipoprotein results in spontaneous particle aggregation and promotes macrophage foam cell formation.

Objective: Secretory phospholipase A2 (sPLA2) enzymes hydrolyze the sn-2 fatty acyl ester bond of phospholipids to produce a free fatty acid and a lysophospholid. Group V sPLA2 is expressed in cultured macrophage cells and has high affinity for phosphatidyl choline-containing substrates. The present study assesses the presence of group V sPLA2 in human and mouse atherosclerotic lesions and its activity toward low-density lipoprotein (LDL) particles.

Alcohol, but not lipopolysaccharide-induced liver apoptosis involves changes in intracellular compartmentalization of apoptotic regulators.

Background: While alcohol-induced augmentation of liver apoptosis has been demonstrated in humans and laboratory animals, the underlying mechanisms are not fully elucidated. This study addresses the question whether alcohol and bacterial lipopolysaccharide (LPS), a putative mediator of alcohol effects on the liver, induce augmentation of liver apoptosis by intrinsic or extrinsic signaling pathways. This information may prove important for future design of therapies for alcoholic liver disease.