Ceramide activates microglia to enhance the production/secretion of brain-derived neurotrophic factor (BDNF) without induction of deleterious factors in vitro

J Neurochem. 2002 Feb;80(4):697-705. doi: 10.1046/j.0022-3042.2001.00752.x.

Abstract

In analyzing the regulation of neurotrophin production/secretion from microglia, C8-ceramide (D-erythro-sphingosine, N-octanoyl-) was found to induce secretion of brain-derived neurotrophic factor (BDNF) from microglia in vitro. In the present study, the action of C8-ceramide in secreting neurotrophic and harmful factors was investigated and compared with the effects of lipopolysaccharide (LPS). C8-ceramide as well as LPS enhanced the production/secretion of BDNF but, different from LPS, did not induce tumor necrosis factor alpha, interleukin-1beta, or nitric oxide. The C8-ceramide-induced BDNF release was significantly suppressed by protein kinase C (PKC) inhibitor, bisindolylmaleimide, which targets PKC isoforms, alpha, beta, gamma, delta and epsilon. However, it was not suppressed by a specific inhibitor of PKCalpha. Furthermore, PKCbeta and gamma were undetected in the microglia. Therefore, PKCdelta and/or epsilon appear to be functioning PKC isoforms. In contrast, none of the mitogen-activated protein kinases (MAPKs) and none of the transcription factors, including the cAMP response element-binding transcription factor (CREB) and nuclear factor kappaB (NFkappaB) were activated in the microglia in response to C8-ceramide. These results indicate that ceramide-induced BDNF release in microglia is mediated by a signaling pathway associated with PKCdelta and/or epsilon, but not with activation of MAPKs, CREB and NFkappaB.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain-Derived Neurotrophic Factor / biosynthesis*
  • Brain-Derived Neurotrophic Factor / genetics
  • Brain-Derived Neurotrophic Factor / metabolism*
  • Cells, Cultured
  • Ceramides / pharmacology*
  • Enzyme Activation / drug effects
  • Enzyme Inhibitors / pharmacology
  • Interleukin-1 / analysis
  • Interleukin-1 / biosynthesis
  • Interleukin-1 / metabolism
  • Lipopolysaccharides / pharmacology
  • Microglia / cytology
  • Microglia / drug effects*
  • Microglia / metabolism*
  • Mitogen-Activated Protein Kinases / metabolism
  • Nerve Growth Factor / analysis
  • Nerve Growth Factor / biosynthesis
  • Nerve Growth Factor / metabolism
  • Nerve Growth Factors / analysis
  • Nerve Growth Factors / biosynthesis
  • Nerve Growth Factors / metabolism
  • Plasminogen / metabolism
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase C / metabolism
  • RNA, Messenger / analysis
  • RNA, Messenger / metabolism
  • Rats
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transcription Factors / metabolism
  • Tumor Necrosis Factor-alpha / analysis
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Brain-Derived Neurotrophic Factor
  • Ceramides
  • Enzyme Inhibitors
  • Interleukin-1
  • Lipopolysaccharides
  • Nerve Growth Factors
  • RNA, Messenger
  • Transcription Factors
  • Tumor Necrosis Factor-alpha
  • Plasminogen
  • Nerve Growth Factor
  • Protein Kinase C
  • Mitogen-Activated Protein Kinases