Induction of COX-2 by LPS in macrophages is regulated by Tpl2-dependent CREB activation signals

EMBO J. 2002 Sep 16;21(18):4831-40. doi: 10.1093/emboj/cdf478.

Abstract

Macrophage activation by bacterial lipopolysaccharide (LPS) promotes the secretion of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta), and of secondary mediators, such as leukotrienes and prostaglandins (PGs). Mice lacking the gene encoding the serine/threonine protein kinase Tpl2/Cot produce low levels of TNF-alpha in response to LPS because of an ERK-dependent post-transcriptional defect, and they are resistant to LPS/D-galactosamine-induced endotoxin shock. In this study we demonstrate that prostaglandin E2 and its regulatory enzyme, COX-2, are also targets of Tpl2-transduced LPS signals in bone marrow-derived mouse macrophages. Thus, LPS-stimulated Tpl2(-/-) macrophages express low levels of COX-2 and PGE2, compared with wild-type Tpl2(+/+) cells. The ability of Tpl2 to regulate COX-2 expression depends on ERK signals that activate p90Rsk and Msk1, which in turn phosphorylate CREB, a key regulator of COX-2 transcription. These data identify physiological targets of Tpl2 signaling downstream of ERK and further implicate Tpl2 in the pathophysiology of inflammation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Line
  • Cyclic AMP Response Element-Binding Protein / metabolism*
  • Cyclooxygenase 2
  • Dinoprostone / metabolism
  • Enzyme Induction
  • Genes, Reporter
  • Glycogen Synthase Kinase 3 / metabolism
  • Inflammation / metabolism
  • Isoenzymes / genetics
  • Isoenzymes / metabolism*
  • Lipopolysaccharides / pharmacology*
  • MAP Kinase Kinase Kinases / genetics
  • MAP Kinase Kinase Kinases / metabolism*
  • Macrophage Activation / physiology*
  • Macrophages / drug effects*
  • Macrophages / metabolism
  • Mice
  • Peroxidases / metabolism
  • Plant Proteins / metabolism
  • Promoter Regions, Genetic
  • Prostaglandin-Endoperoxide Synthases / genetics
  • Prostaglandin-Endoperoxide Synthases / metabolism*
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism*
  • RNA Stability
  • Ribosomal Protein S6 Kinases, 90-kDa / metabolism
  • Signal Transduction / physiology*

Substances

  • Cyclic AMP Response Element-Binding Protein
  • Isoenzymes
  • Lipopolysaccharides
  • Plant Proteins
  • Proto-Oncogene Proteins
  • Peroxidases
  • Cyclooxygenase 2
  • Prostaglandin-Endoperoxide Synthases
  • Ribosomal Protein S6 Kinases, 90-kDa
  • MAP Kinase Kinase Kinases
  • Map3k8 protein, mouse
  • Glycogen Synthase Kinase 3
  • Msk-1 protein, Medicago sativa
  • Dinoprostone