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Article: Nonselective inhibition of neutrophil functions by sphinganine

TitleNonselective inhibition of neutrophil functions by sphinganine
Authors
Issue Date1987
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal of Biological Chemistry, 1987, v. 262 n. 21, p. 10072-10076 How to Cite?
AbstractSphinganine has been proposed to be a specific inhibitor of protein kinase C. In the present study we have evaluated whether sphinganine is a convenient tool to probe for the role of protein kinase C in neutrophil function. Human neutrophils were loaded with the fluorescent probe quin2 and then tested in parallel for cytosolic free Ca2+, [Ca2+]i, membrane potential changes, O2- production, and exocytosis of primary granules (containing beta-glucuronidase) in response to various stimuli. In addition to inhibiting O2- production and exocytosis in a dose-dependent manner, sphinganine also blocked formyl-methionyl-leucyl-phenylalanine-induced [Ca2+]i, transients. Furthermore, sphinganine inhibited exocytosis elicited by the calcium ionophore ionomycin. Although sphinganine blocked O2- production due to phorbol 12-myristate 13-acetate, the most striking finding was that the drug rendered the cells leaky. Thus, at similar concentrations as those inhibiting cellular functions, sphinganine was shown to lead to cell permeabilization, as assessed by release of quin2 and cytoplasmic markers into the extracellular medium, and changes in plasma membrane potential. We conclude, therefore, that sphinganine does not appear to be a suitable compound for the evaluation of the involvement of protein kinase C in neutrophil activation.
Persistent Identifierhttp://hdl.handle.net/10722/195296
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPittet, D-
dc.contributor.authorKrause, KH-
dc.contributor.authorWollheim, CB-
dc.contributor.authorBruzzone, R-
dc.contributor.authorLew, DP-
dc.date.accessioned2014-02-26T06:42:37Z-
dc.date.available2014-02-26T06:42:37Z-
dc.date.issued1987-
dc.identifier.citationJournal of Biological Chemistry, 1987, v. 262 n. 21, p. 10072-10076-
dc.identifier.issn0021-9258-
dc.identifier.urihttp://hdl.handle.net/10722/195296-
dc.description.abstractSphinganine has been proposed to be a specific inhibitor of protein kinase C. In the present study we have evaluated whether sphinganine is a convenient tool to probe for the role of protein kinase C in neutrophil function. Human neutrophils were loaded with the fluorescent probe quin2 and then tested in parallel for cytosolic free Ca2+, [Ca2+]i, membrane potential changes, O2- production, and exocytosis of primary granules (containing beta-glucuronidase) in response to various stimuli. In addition to inhibiting O2- production and exocytosis in a dose-dependent manner, sphinganine also blocked formyl-methionyl-leucyl-phenylalanine-induced [Ca2+]i, transients. Furthermore, sphinganine inhibited exocytosis elicited by the calcium ionophore ionomycin. Although sphinganine blocked O2- production due to phorbol 12-myristate 13-acetate, the most striking finding was that the drug rendered the cells leaky. Thus, at similar concentrations as those inhibiting cellular functions, sphinganine was shown to lead to cell permeabilization, as assessed by release of quin2 and cytoplasmic markers into the extracellular medium, and changes in plasma membrane potential. We conclude, therefore, that sphinganine does not appear to be a suitable compound for the evaluation of the involvement of protein kinase C in neutrophil activation.-
dc.languageeng-
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/-
dc.relation.ispartofJournal of Biological Chemistry-
dc.rightsJournal of Biological Chemistry. Copyright © American Society for Biochemistry and Molecular Biology, Inc.-
dc.rightsThis research was originally published in Journal of Biological Chemistry. Journal of Biological Chemistry, 1987, v. 262 n. 21, p. 10072-10076 © the American Society for Biochemistry and Molecular Biology-
dc.subject.meshNeutrophils - drug effects-
dc.subject.meshPentetic Acid - pharmacology-
dc.subject.meshProtein Kinase C - antagonists and inhibitors-
dc.subject.meshSphingosine - analogs and derivatives - pharmacology-
dc.subject.meshSuperoxides - biosynthesis-
dc.titleNonselective inhibition of neutrophil functions by sphinganineen_US
dc.typeArticleen_US
dc.identifier.emailBruzzone, R: bruzzone@HKUCC.hku.hk-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid3038865-
dc.identifier.scopuseid_2-s2.0-0023187919-
dc.identifier.volume262-
dc.identifier.issue21-
dc.identifier.spage10072-
dc.identifier.epage10076-
dc.identifier.isiWOS:A1987J292500028-
dc.publisher.placeUnited States-

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