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

doi:10.1016/0006-291X(90)90903-Z

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

Microbiology And Immunology

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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.

Original language	English (US)
Pages (from-to)	953-959
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	166
Issue number	2
DOIs	https://doi.org/10.1016/0006-291X(90)90903-Z
State	Published - Jan 30 1990

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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Human cytomegalovirus stimulates arachidonic acid metabolism through pathways that are affected by inhibitors of phospholipase A2 and protein kinase C. / AbuBakar, Sazaly; Boldogh, Istvan; Albrecht, Thomas.
In: Biochemical and Biophysical Research Communications, Vol. 166, No. 2, 30.01.1990, p. 953-959.

Research output: Contribution to journal › Article › peer-review

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

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.",

author = "Sazaly AbuBakar and Istvan Boldogh and Thomas Albrecht",

note = "Funding Information: These studies were supported by USEPA research grants R81 2086 and R81 5048. S. AbuBakar is the recipient of a J.W. McLaughlin Fellowship and American Lung Association/San Jacinto Area Research Scholarship.",

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N1 - Funding Information: These studies were supported by USEPA research grants R81 2086 and R81 5048. S. AbuBakar is the recipient of a J.W. McLaughlin Fellowship and American Lung Association/San Jacinto Area Research Scholarship.

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

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