Tumor necrosis factor alpha augments the expression of glucose-6-phosphate dehydrogenase in rat hepatic endothelial and Kupffer cells.
Tumor necrosis factor alpha augments the expression of glucose-6-phosphate dehydrogenase in rat hepatic endothelial and Kupffer cells.
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DOI：
10.1016/s0024-3205(96)00641-8
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发表时间：
1997-01
期刊：
影响因子：
6.1
通讯作者：
Z. Spolarics;J. X. Wu
中科院分区：
文献类型：
--
作者：
Z. Spolarics;J. X. Wu
Cellular activity of glucose-6-phosphate dehydrogenase (G6PD), the key enzyme of the hexose monophosphate shunt, supports several pathways involved in the nonspecific immune response. In the present study, we investigated the in vivo effects of selected pro-inflammatory cytokines on the expression of G6PD in Kupffer and hepatic endothelial cells. Murine recombinant TNFα, IL-lβ, or IL-6 (1.5 × 105U/kg) was injected and cellular G6PD mRNA level determined using a quantitative reverse transcription and polymerase chain reaction method. G6PD mRNA was elevated two- to threefold seven hours after the injection of TNFa in Kupffer and endothelial cells as compared to cells from saline-injected animals. The elevated G6PD mRNA was accompanied by increased cellular enzyme activity in both cells. The cellular activity of 6-phosphogluconate dehydrogenase (6PGD) was also increased seven hours after TNFα treatment in these cells. G6PD mRNA and enzyme activity returned to control levels 22h after TNFa administration. In contrast to the marked effects of TNFα, no significant alterations were found on G6PD expression following IL-1β or IL-6 injections in these cells. None of these cytokines caused changes in G6PD or 6PGD expression in parenchymal cells. These data indicate that the proinflammatory cytokine TNFα plays an important role in the regulation of cellular G6PD expression in hepatic immune competent cells.
