Human cytomegalovirus stimulates arachidonic acid metabolism through pathways that are affected by inhibitors of phospholipase A2 and protein kinase C

Sazaly AbuBakar, Istvan Boldogh, Thomas Albrecht

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

Inhibitors of phospholipase A2, tetracaine and quinacrine, inhibitors of protein kinases, H-7 and H-8, and a diacylglycerol lipase inhibitor reduced the level of CMV-induced [3H]AA release. A combination of H-7 and quinacrine inhibited stimulation of [3H]AA by about 80%. LU cells chronically treated with TPA and infected with CMV, had a reduced level of CMV-induced [3H]AA release and in the presence of quinacrine it was completely inhibited. These results suggest that CMV-induced stimulation of AA metabolism is mediated by pathways which are associated with activation of PLA2 and protein kinase C.

Original languageEnglish (US)
Pages (from-to)953-959
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume166
Issue number2
DOIs
StatePublished - Jan 30 1990

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Phospholipase A2 Inhibitors
Quinacrine
Cytomegalovirus
Arachidonic Acid
Metabolism
Protein Kinase C
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
Tetracaine
Lipoprotein Lipase
Protein Kinase Inhibitors
Chemical activation

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

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abstract = "Inhibitors of phospholipase A2, tetracaine and quinacrine, inhibitors of protein kinases, H-7 and H-8, and a diacylglycerol lipase inhibitor reduced the level of CMV-induced [3H]AA release. A combination of H-7 and quinacrine inhibited stimulation of [3H]AA by about 80{\%}. LU cells chronically treated with TPA and infected with CMV, had a reduced level of CMV-induced [3H]AA release and in the presence of quinacrine it was completely inhibited. These results suggest that CMV-induced stimulation of AA metabolism is mediated by pathways which are associated with activation of PLA2 and protein kinase C.",
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AU - Albrecht, Thomas

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AB - Inhibitors of phospholipase A2, tetracaine and quinacrine, inhibitors of protein kinases, H-7 and H-8, and a diacylglycerol lipase inhibitor reduced the level of CMV-induced [3H]AA release. A combination of H-7 and quinacrine inhibited stimulation of [3H]AA by about 80%. LU cells chronically treated with TPA and infected with CMV, had a reduced level of CMV-induced [3H]AA release and in the presence of quinacrine it was completely inhibited. These results suggest that CMV-induced stimulation of AA metabolism is mediated by pathways which are associated with activation of PLA2 and protein kinase C.

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