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Identification of protein kinase C isoforms involved in interferon-gamma-induced expression of inducible nitric oxide synthase in murine BV2 microglia.

Kang, J; Yang, M; Jou, I; Joe, E
Neuroscience letters, 299(3):205-208, 2001
Journal Title
Neuroscience letters
Microglia are major inflammatory cells of the brain. It has been known that interferon-gamma (IFN-gamma) induces nitric oxide (NO)/inducible nitric oxide synthase (iNOS) in microglia, and that protein kinase C (PKC) mediates the action of IFN-gamma. In this study, we investigated isoforms of PKC that are involved in IFN-gamma-induced activation of microglia using BV2 murine microglial cells. NO release/iNOS expression in IFN-gamma -treated BV2 cells was reduced in the presence of PKC inhibitors (Gö 6976 and BIM), and by long-term pre-treatment (48 h) of cells with phorbol-12-myristate-13-acetate (PMA) or thymeleatoxin. PMA depleted alpha, beta, delta, and epsilon isoforms, and thymeleatoxin depleted alpha, beta, and epsilon isoforms although gamma, eta, iota, lambda, theta, mu, and zeta were also detected in these cells. Furthermore, IFN-gamma phosphorylated alpha and epsilon on their tyrosine residues. These results suggested that alpha and epsilon could be the major PKC isoforms involved in signaling pathways of IFN-gamma to induce NO/iNOS expression in BV2 microglia.
MeSH terms
AnimalsCell Line/drug effectsCell Line/enzymologyEncephalitis/enzymology*Encephalitis/physiopathologyInterferon-gamma/metabolism*Interferon-gamma/pharmacologyMiceMicroglia/drug effectsMicroglia/enzymology*Nerve Degeneration/enzymologyNerve Degeneration/physiopathologyNitric Oxide Synthase/drug effectsNitric Oxide Synthase/metabolism*Phosphorylation/drug effectsProtein Isoforms/drug effectsProtein Isoforms/metabolismProtein Kinase C/drug effectsProtein Kinase C/metabolism*Tyrosine/metabolism
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Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
AJOU Authors
주, 일로조, 은혜
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