Hmgi-c-independent Activation of MuRantes in Vivo

Cell Growth Differ. 2002 Jan;13(1):39-45.

Abstract

The architectural factor HMGI-C is of considerable interest for its recognized roles in mammalian development and tumorigenesis. As a result, the identification of downstream target genes of HMGI-C is the present focus of active research. In vitro evidence from macrophage cell lines has previously suggested that Hmgi-c is necessary for the inducible activation of MuRantes expression. To attempt to verify this hypothesis, an in vivo analysis was performed that took advantage of the existence of the Hmgi-c null mouse strain. The ability of cells and tissues extracted from Hmgi-c null mice to express the inflammatory chemokine MuRantes was investigated. The investigation examined MuRantes expression in primary embryonic fibroblasts and fresh peritoneal macrophages after Newcastle disease virus induction and whole organs after lipopolysaccharide induction. Each of these systems clearly demonstrates that Hmgi-c is not required for the activation of MuRantes expression.

MeSH terms

  • Animals
  • Blotting, Northern
  • Cells, Cultured
  • Chemokine CCL5 / biosynthesis
  • Chemokine CCL5 / metabolism*
  • Embryo, Mammalian / cytology
  • Escherichia coli / genetics
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism
  • Gene Expression Regulation, Developmental
  • Genotype
  • HMGA2 Protein / genetics
  • HMGA2 Protein / metabolism*
  • Lipopolysaccharides / pharmacology
  • Macrophages, Peritoneal / drug effects
  • Macrophages, Peritoneal / metabolism
  • Male
  • Mice
  • Mice, Knockout
  • Newcastle disease virus / genetics
  • Recombinant Proteins / genetics
  • Recombinant Proteins / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tissue Distribution
  • Transfection

Substances

  • Chemokine CCL5
  • HMGA2 Protein
  • Lipopolysaccharides
  • Recombinant Proteins