Inhibition of microglial inflammation by the MLK inhibitor CEP-1347.

Research output: Contribution to journalJournal articleResearchpeer-review

  • Søren Lund
  • Peter Porzgen
  • Anne Louise Mortensen
  • Hasseldam, Henrik
  • Donna Bozyczko-Coyne
  • Siegfried Morath
  • Thomas Hartung
  • Marina Bianchi
  • Pietro Ghezzi
  • Malika Bsibsi
  • Sipke Dijkstra
  • Marcel Leist
CEP-1347 is a potent inhibitor of the mixed lineage kinases (MLKs), a distinct family of mitogen-activated protein kinase kinase kinases (MAPKKK). It blocks the activation of the c-Jun/JNK apoptotic pathway in neurons exposed to various stressors and attenuates neurodegeneration in animal models of Parkinson's disease (PD). Microglial activation may involve kinase pathways controlled by MLKs and might contribute to the pathology of neurodegenerative diseases. Therefore, the possibility that CEP-1347 modulates the microglial inflammatory response [tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and monocyte chemotactic protein-1 (MCP-1)] was explored. Indeed, the MLK inhibitor CEP-1347 reduced cytokine production in primary cultures of human and murine microglia, and in monocyte/macrophage-derived cell lines, stimulated with various endotoxins or the plaque forming peptide Abeta1-40. Moreover, CEP-1347 inhibited brain TNF production induced by intracerebroventricular injection of lipopolysaccharide in mice. As expected from a MLK inhibitor, CEP-1347 acted upstream of p38 and c-Jun activation in microglia by dampening the activity of both pathways. These data imply MLKs as important, yet unrecognized, modulators of microglial inflammation, and demonstrate a novel anti-inflammatory potential of CEP-1347.
Original languageEnglish
JournalJournal of Neurochemistry
Volume92
Issue number6
Pages (from-to)1439-51
Number of pages12
ISSN0022-3042
DOIs
Publication statusPublished - 2005
Externally publishedYes

Bibliographical note

Keywords: Animals; Anti-Inflammatory Agents; Carbazoles; Cell Line; Cells, Cultured; Cytokines; Down-Regulation; Encephalitis; Enzyme Inhibitors; Gliosis; Humans; Indoles; Inflammation Mediators; JNK Mitogen-Activated Protein Kinases; MAP Kinase Kinase Kinases; Mice; Mice, Inbred C57BL; Microglia; Trans-Activation (Genetics); Tumor Necrosis Factor-alpha; p38 Mitogen-Activated Protein Kinases

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