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• W2213239530 endingPage "C914" @default.
• W2213239530 startingPage "C906" @default.
• W2213239530 abstract "We addressed the role of protein kinase C (PKC) isozymes in mediating tumor necrosis factor-alpha (TNF-alpha)-induced oxidant generation in endothelial cells, a requirement for nuclear factor-kappaB (NF-kappaB) activation and intercellular adhesion molecule-1 (ICAM-1) gene transcription. Depletion of the conventional (c) and novel (n) PKC isozymes following 24 h exposure of human pulmonary artery endothelial (HPAE) cells with the phorbol ester, phorbol 12-myristate 13-acetate (500 nM), failed to prevent TNF-alpha-induced oxidant generation. In contrast, inhibition of PKC-zeta synthesis by the antisense oligonucleotide prevented the oxidant generation following the TNF-alpha stimulation. We observed that PKC-zeta also induced the TNF-alpha-induced NF-kappaB binding to the ICAM-1 promoter and the resultant ICAM-1 gene transcription. We showed that expression of the dominant negative mutant of PKC-zeta prevented the TNF-alpha-induced ICAM-1 promoter activity, whereas overexpression of the wild-type PKC-zeta augmented the response. These data imply a critical role for the PKC-zeta isozyme in regulating TNF-alpha-induced oxidant generation and in signaling the activation of NF-kappaB and ICAM-1 transcription in endothelial cells." @default.
• W2213239530 created "2016-06-24" @default.
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• W2213239530 date "2000-10-01" @default.
• W2213239530 modified "2023-09-24" @default.
• W2213239530 title "Protein kinase C-ζ mediates TNF-α-induced ICAM-1 gene transcription in endothelial cells" @default.
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• W2213239530 doi "https://doi.org/10.1152/ajpcell.2000.279.4.c906" @default.
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