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• W2009703010 abstract "Phospholipase A2(PLA2) activity has been suggested to mediate some of the tumor necrosis factor (TNF) induced cellular responses including cytotoxicity. We evaluated the induction of both the 85-kDa cytosolic phospholipase A2 (cPLA2) and non-pancreatic group II PLA2 gene expression by TNF-α in a human bronchial epithelial cell line (BEAS 2B cell). TNF-α (20 ng/ml) induced a significantly increased release of prelabeled [3H]arachidonic acid (AA) following 4–24 h incubation. Calcium ionophore A23187 (10−5 M) further increased the [3H]AA release from the TNF-α -treated cells. In vitro activity assay revealed that TNF-α increased the dithiothreitol (DTT)-resistant PLA2 activity which was blocked by the cPLA2 inhibitor AACOCF3. Treatment with TNF-a for 4–24 h increased the cPLA2 protein and mRNA levels which were blocked by the broad inhibitor of protein kinases staurosporine, the protein kinase C (PKC) inhibitor calphostin C, and to a lesser extent the calcium/calmodulin-dependent protein kinase inhibitor W-7. Reverse transcription and polymerase chain reaction amplification of the group II PLA2 mRNA showed that it is expressed in human lung but not in the bronchial epithelial cell line. TNF-α failed to induce the expression of group II PLA2 in the BEAS 213 cells. These results demonstrate that the cPLA2 gene expression is up-regulated by TNF-α and this effect may contribute to the TNF-α stimulated AA release in airway epithelial cells." @default.
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• W2009703010 date "1996-02-01" @default.
• W2009703010 modified "2023-09-27" @default.
• W2009703010 title "Tumor necrosis factor-α induces the 85-kDa cytosolic phospholipase A2 gene expression in human bronchial epithelial cells" @default.
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• W2009703010 doi "https://doi.org/10.1016/0167-4889(95)00143-3" @default.
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