Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1997-3-25
pubmed:abstractText
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 TNF alpha, IL-1 beta, or IL-6 (1.5 x 10(5) U/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 TNF alpha 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 TNF alpha treatment in these cells. G6PD mRNA and enzyme activity returned to control levels 22h after TNF alpha administration. In contrast to the marked effects of TNF alpha, no significant alterations were found on G6PD expression following IL-1 beta 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 TNF alpha plays an important role in the regulation of cellular G6PD expression in hepatic immune competent cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
565-71
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Tumor necrosis factor alpha augments the expression of glucose-6-phosphate dehydrogenase in rat hepatic endothelial and Kupffer cells.
pubmed:affiliation
Department of Anatomy, Cell Biology and Injury Sciences, University of Medicine and Dentistry of New Jersey, Newark, USA. spolaric@umdnj.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.