Record number :
519266
Title of article :
Attenuating effects of heat shock against TGF-β1-induced apoptosis in cultured rat hepatocytes
Author/Authors :
Carmen D?ez-Fern?ndez، نويسنده , , David Andrés، نويسنده , , Mar?a Cascales، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2002
Pages :
12
From page :
835
To page :
846
Abstract :
Heat shock proteins (HSPs) induction confers protection against diverse forms of cellular injury. However, the mechanism by which HSPs exert cytoprotective effects remains unclear. Treatment of rat hepatocyte with transforming growth factor-β1 (TGF-β1) induces growth arrest followed by extensive cell death by apoptosis. In this study, the effects of preexposure to heat on TGF-β1-induced apoptosis of cultured hepatocytes were examined. Treatment of hepatocytes for 24 h with TGF-β1 resulted in significant apoptotic cell death, as demonstrated by DNA fragmentation, caspase activation, and hypodiploid DNA peak. Moreover, TGF-β1-induced cell death was accompanied by an enhanced generation of reactive oxygen species and a loss of the mitochondrial membrane potential. These effects were attenuated when the hepatocytes were subjected to 43°C for 20 min prior to the cytokine stimulation. The enhancement in HSP70 expression at mRNA and protein levels induced by heat preexposure was accompanied by an increase in mRNA levels of intracellular antioxidant enzymes. Heat treatment also prevented TGF-β1-induced activation of nuclear factor κ B (NF-κB) by preventing the degradation of the inhibitory protein κ Bα (IκBα). In conclusion, these data indicate that in the mechanism by which a mild heat pretreatment increases the resistance of hepatocytes to TGF-β1-induced apoptotic cell death, the upregulation of catalase expression and a decrease in ROS generation are involved.
Keywords :
antioxidant enzymes , heat shock proteins , Nuclear factor ? B , Reactive oxygen species , Apoptosis , free radicals
Journal title :
Free Radical Biology and Medicine
Serial Year :
2002
Link To Document :
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