Hypoxia-reoxygenation differentially stimulates stress-activated protein kinases in primary-cultured rat hepatocytes

Organ injury after ischemia and reperfusion (I/R) remains one of the most important limiting factors in liver surgery and transplantation. Oxygen-free radical (OFR) generation is considered a major cause of this damage. JNK1/SAPK1, a member of MAPK family, regulates cell adaptation to stressful cond...

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Bibliographic Details
Published in:Transplant international 2000, Vol.13 Suppl 1, p.S597-S599
Main Authors: Crenesse, D, Schmid-Alliana, A, Hornoy, J, Rossi, B, Gugenheim, J
Format: Article
Language:English
Subjects:
Animals
Cell Hypoxia - physiology
Cells, Cultured
Enzyme Activation
Hepatocytes - cytology
Hepatocytes - enzymology
Hepatocytes - physiology
Male
Mitogen-Activated Protein Kinase 8
Mitogen-Activated Protein Kinases - metabolism
Oxidative Stress - physiology
Rats
Rats, Wistar
Temperature
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Summary:Organ injury after ischemia and reperfusion (I/R) remains one of the most important limiting factors in liver surgery and transplantation. Oxygen-free radical (OFR) generation is considered a major cause of this damage. JNK1/SAPK1, a member of MAPK family, regulates cell adaptation to stressful conditions. The aim of this study was to determine if hypoxia-reoxygenation (H/R) can activate JNK1/SAPK1 and if OFR are involved in this activation. Primary cultured rat hepatocytes isolated from other liver cells and blood flow were submitted to warm and cold H/R phases mimicking surgical and transplant conditions. JNK1/SAPK1 was activated by both warm and cold H/R. Deferoxamine (1 mM), di-phenyleneiodonium (50 microM) and N-acetylcysteine (10 mM) significantly inhibited this kinase activation.
ISSN:0934-0874
1432-2277
DOI:10.1007/s001470050410