Regulation of Kupffer cell TNF gene expression during experimental acute pancreatitis: The role of p38-MAPK, ERK1/2, SAPK/JNK, and NF-[kappa]B

We have demonstrated that Kupffer cell-derived tumor necrosis factor (TNF) mediates pancreatitis-associated liver injury. The aim of this study was to determine the role of p38 mi to gen-activated protein kinase (MAPK), extracellular stress-related kinase 1/2 (ERK1/2), stress-activated protein kinas...

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Bibliographic Details
Published in:Journal of gastrointestinal surgery 2003-02, Vol.7 (1), p.20
Main Authors: Murr, Michel M, Yang, Jun, Fier, Adam, Gallagher, Scott F, Carter, Gay, Gower, William R, Norman, James G
Format: Article
Language:English
Subjects:
Cells
Gene expression
Kinases
Proteins
Rodents
Online Access:Get full text
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Summary:We have demonstrated that Kupffer cell-derived tumor necrosis factor (TNF) mediates pancreatitis-associated liver injury. The aim of this study was to determine the role of p38 mi to gen-activated protein kinase (MAPK), extracellular stress-related kinase 1/2 (ERK1/2), stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), and nuclear factor-KB (NF-ΚB) in TNF gene expression within Kupffer cells. TNF and TNF-mRNA were measured in rat livers perfused with elastase. TNF, TNF-mRNA, NF-B activation, and phosphorylated p38-MAPK, SAPK/JNK, and ERK1/2 were determined in Kupffer cells treated with elastase. Elastase increased TNF and upregulated TNF-mRNA in livers (P
ISSN:1091-255X
1873-4626
DOI:10.1016/S1091-255X(02)00053-7