Activation of survival and apoptotic signaling pathways in lymphocytes exposed to XXXX .

@entity1 @entity137 @entity14839 @entity6 @entity4674 @entity3963 @entity8277 @entity412 @entity2368 @entity1435 @entity35 @entity413 @entity7609 @entity2383
The @entity137 of @entity7609 (PA) towards a @entity1 T-lymphocyte cell line (Jurkat) has been previously investigated but the mechanism(s) of PA action were unknown. In the current study, Jurkat cells were treated with sub-lethal concentrations of PA (50-150  M) and the activity of various signaling proteins was investigated. PA-induced apoptosis and @entity2383 in a dose-dependent manner as evaluated by DNA fragmentation assay and depolarization of the mitochondrial membrane, respectively. PA treatment provoked release of @entity4674 from the inner mitochondrial membrane to the cytosol, activated members of the MAPK protein family JNK, @entity1435 , @entity3963 , activated caspases 3/9, and increased oxidative/nitrosative stress. Exposure of cells to PA for 12 h increased @entity8277 ( @entity8277 ) and @entity2368 levels in the plasma membrane. Insulin treatment (10 mU/ml/30 min) increased the phosphorylation of the IR b-subunit and Akt. A correlation was found between DNA fragmentation and expression levels of both @entity8277 and @entity2368 . Similar results were obtained for PA-treated lymphocytes from healthy @entity1 donors and from mesenteric lymph nodes of 48-h starved @entity35 . PA stimulated @entity413 uptake by Jurkat cells (in the absence of insulin), stimulated accumulation of neutral lipids ( @entity412 ), and other lipid classes (phospholipids and @entity14839 ) but reduced @entity413 oxidation. Our results suggest that parameters of insulin signaling and non-oxidative @entity413 metabolism are stimulated as part of a coordinated response to prompt survival in lymphocytes exposed to PA but at higher concentrations, apoptosis prevails. These findings may explain aspects of lymphocyte dysfunction associated with @entity6 .
