Bone morphogenetic protein-7 inhibits constitutive and interleukin-1 beta-induced monocyte chemoattractant protein-1 expression in human mesangial cells: role for JNK/AP-1 pathway

J Immunol. 2003 Mar 1;170(5):2557-63. doi: 10.4049/jimmunol.170.5.2557.

Abstract

Bone morphogenetic protein-7 (BMP-7), which belongs to the TGF-beta superfamily, has been shown to reduce macrophage infiltration and tissue injury in animal models of inflammatory renal disease. To explore the mechanism involved in the anti-inflammatory effect, we investigated the effect of BMP-7 on monocyte chemoattractant protein-1 (MCP-1) expression in cultured human mesangial cells. BMP- 7 significantly inhibited constitutive and IL-1 beta-induced MCP-1 protein production and MCP-1 mRNA expression by mesangial cells in a time- and concentration-dependent manner. BMP-7 also inhibited IL-1 beta-induced monocyte chemotactic activity released from the mesangial cells. We examined the role of transcription factors NF-kappa B and AP-1 in BMP-7 inhibition of IL-1 beta-induced MCP-1 expression. IL-1 beta increased NF-kappa B and AP-1 activity and both transcription factors mediated IL-1 beta-induced MCP-1 expression in mesangial cells. BMP-7 inhibited IL-1 beta-induced AP-1 activity in a concentration-dependent manner. In contrast, IL-1 beta-induced NF-kappa B activity and I kappa B alpha degradation were not affected by BMP-7. Furthermore, IL-1 beta-induced phosphorylation of c-Jun N-terminal kinase was inhibited by BMP-7. These data suggest that BMP-7 inhibits constitutive and IL-1 beta-induced MCP-1 expression in human mesangial cells partly by inhibiting c-Jun N-terminal kinase activity and subsequent AP-1 activity, and provide new insight into the therapeutic potential of BMP-7 in the inflammatory renal diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bone Morphogenetic Protein 7
  • Bone Morphogenetic Proteins / pharmacology
  • Bone Morphogenetic Proteins / physiology*
  • Cells, Cultured
  • Chemokine CCL2 / antagonists & inhibitors*
  • Chemokine CCL2 / biosynthesis*
  • Chemokine CCL2 / metabolism
  • Chemokine CCL2 / physiology
  • Enzyme Inhibitors / pharmacology
  • Glomerular Mesangium / cytology
  • Glomerular Mesangium / enzymology
  • Glomerular Mesangium / immunology*
  • Glomerular Mesangium / metabolism
  • Humans
  • Interleukin-1 / antagonists & inhibitors
  • Interleukin-1 / pharmacology*
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • Mitogen-Activated Protein Kinases / metabolism
  • Mitogen-Activated Protein Kinases / physiology*
  • NF-kappa B / antagonists & inhibitors
  • NF-kappa B / metabolism
  • Phosphorylation
  • Protein Synthesis Inhibitors / pharmacology
  • RNA, Messenger / antagonists & inhibitors
  • RNA, Messenger / biosynthesis
  • Recombinant Proteins / pharmacology
  • Signal Transduction / immunology*
  • Transcription Factor AP-1 / antagonists & inhibitors
  • Transcription Factor AP-1 / metabolism
  • Transcription Factor AP-1 / physiology*
  • Transforming Growth Factor beta*

Substances

  • BMP7 protein, human
  • Bone Morphogenetic Protein 7
  • Bone Morphogenetic Proteins
  • Chemokine CCL2
  • Enzyme Inhibitors
  • Interleukin-1
  • NF-kappa B
  • Protein Synthesis Inhibitors
  • RNA, Messenger
  • Recombinant Proteins
  • Transcription Factor AP-1
  • Transforming Growth Factor beta
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases