NDLI: Inhibition of classical PKC isoenzymes downregulates STAT1 activation and iNOS expression in LPS-treated murine J774 macrophages

Content Provider	PubMed Central
Author	Salonen, Tiina Sareila, Outi Jalonen, Ulla Kankaanranta, Hannu Tuominen, Raimo Moilanen, Eeva
Copyright Year	2006
Abstract	Proinflammatory cytokines and bacterial products trigger inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) production in inflammatory and tissue cells. In inflammation, NO acts as an important mediator having both proinflammatory and destructive effects. Protein kinase C (PKC) is a family of serine–threonine protein kinase isoenzymes involved in signal transduction pathways related to inflammatory responses. The aim of the present study was to investigate the role of classical PKC (cPKC) isoenzymes in the regulation of iNOS expression and NO production in murine J774 macrophages and the mechanisms involved. RO318220 (inhibits PKCβ, PKCγ and PKCɛ), GÖ6976 (inhibits cPKC isoenzymes PKCα and PKCβ) and LY333531 (inhibits PKCβ) reduced lipopolysaccharide (LPS)-induced NO production and iNOS expression in a dose-dependent manner as did 6 h pretreatment with 1 μ M phorbol 12-myristate 13-acetate (PMA) (which was shown to downregulate PKC expression). PKC inhibitors also reduced LPS-induced iNOS mRNA levels, but they did not affect the half-life of iNOS mRNA. PKC inhibitors did not alter LPS-induced activation of NF-κB as measured by electrophoretic mobility shift assay. All PKC inhibitors used and pretreatment with 1 μ M PMA inhibited signal transducer and activator of transcription 1 (STAT1) activation as measured by the translocation of STAT1α from the cytosol to the nucleus by Western blot. In addition, inhibition of STAT1 activation by AG-490, an inhibitor of JAK-2, also reduced NO production. These results suggest that cPKC isoenzymes, especially PKCβ, mediate the upregulation of iNOS expression and NO production in activated macrophages in an NF-κB-independent manner, possibly through the activation of transcription factor STAT1.
Related Links	http://dx.doi.org/10.1038/sj.bjp.0706672
Ending Page	799
Page Count	10
Starting Page	790
File Format	PDF
ISSN	00071188
e-ISSN	14765381
Journal	British Journal of Pharmacology
Issue Number	7
Volume Number	147
Language	English
Publisher	Nature Publishing Group
Publisher Date	2006-04-01
Access Restriction	Open
Rights Holder	Nature Publishing Group
Subject Keyword	Pharmacology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Pharmacology

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