Activation of signal transducer and activator of transcription 3 in rat liver after heat shock and reperfusion stress.

Changes in transcription factors (TFs) accompany many types of cell stresses. By using electrophoretic mobility assays we show that the DNA binding of signal transducer and activator of transcription 3 (STAT3) is activated in rat liver by heat shock and ischemia-reperfusion. Northern blot and Western blot analysis reveal an increase of the mRNA and protein level of this transcription factor.

Transferrin receptor gene expression and transferrin-bound iron uptake are increased during postischemic rat liver reperfusion.

Iron-catalyzed production of reactive oxygen species is a cause of liver injury after ischemia/reperfusion (I/R). The aim of the present study was to address the regulation of transferrin receptor (TfR), which mediates cellular iron uptake, during I/R. The molecular mechanisms controlling TfR gene expression in vivo during I/R of rat liver were investigated by molecular biology procedures.

Activation of transcription factors by drugs inducing oxidative stress in rat liver.

Chemically induced oxidative stress of the liver associates with gene reprogramming and activation of some transcription factors (TFs), in particular nuclear factor-kappaB (NF-kappaB). We have now investigated other TFs, such as activator protein-1 (AP-1) and hypoxia inducible factor-1 (HIF-1) that we had shown to be activated in rat liver during heat shock, ischemia or post-ischemic reperfusion, and signal transducer and activator of transcription (STAT), CCAAT/enhancer binding protein (C/EBP) and hepatocyte nuclear factor-1 (HNF-1), which may be involved in the response of the liver to injury. The expression of target genes, containing consensus sequences for these TFs was assessed by Northern and Western blot analysis.

Biomolecular and biochemical response of myocardial cell to ischemia and reperfusion in the course of heart surgery.

Background: Previous studies have shown that biomolecular and biochemical adaptive changes antagonize oxidative damage due to hypoxia and ischemia in myocardial cells. The aim of our study was to verify in human ischemic and reperfused cardiac tissue the relationship between mitochondrial enzyme activities and the activation of HSP70 and c-fos syntheses in the context of a cytoprotective mechanism. Nitric oxide (NO) modulating effects on mitochondrial respiratory chain enzyme activities in ischemic and reperfused tissue were investigated (preliminary report).

Influence of proteasome and redox state on heat shock-induced activation of stress kinases, AP-1 and HSF.

We studied the pattern of activation of stress kinases and of transcription factors activator protein-1 (AP-1) and heat shock factor (HSF) in FAO cells by combining two treatments, i.e. heating (42 degrees C for 1 h) and proteasome inhibition, each known to cause cellular heat shock response.