Regulation of annexin I in rheumatoid synovial cells by glucocorticoids and interleukin-1

Mediators Inflamm. 2006;2006(2):73835. doi: 10.1155/MI/2006/73835.

Abstract

The glucocorticoid (GC)-induced antiinflammatory molecule annexin I is expressed in leukocytes and has antiinflammatory effects in animal models of arthritis, but the expression of annexin I in rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS) is unknown. We report the constitutive and dexamethasone (DEX)-inducible expression of annexin I in RA FLS. DEX increased FLS annexin I protein translocation and mRNA expression. Interleukin (IL)-1beta also induced annexin I translocation and mRNA but also increased intracellular protein. DEX and IL-1 had additive effects on annexin I mRNA, but DEX inhibited the inducing effect of IL-1beta on cell surface annexin I. These results indicate that glucocorticoids and IL-1beta upregulate the synthesis and translocation of annexin I in RA FLS, but interdependent signalling pathways are involved.

MeSH terms

  • Annexin A1 / biosynthesis*
  • Anti-Inflammatory Agents / pharmacology
  • Arthritis, Rheumatoid / metabolism*
  • Dexamethasone / pharmacology
  • Fibroblasts / metabolism*
  • Flow Cytometry
  • Glucocorticoids / metabolism*
  • Humans
  • Interleukin-1 / biosynthesis*
  • Interleukin-1beta / metabolism
  • Protein Transport
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • Synovial Membrane / cytology*
  • Synovial Membrane / metabolism*

Substances

  • Annexin A1
  • Anti-Inflammatory Agents
  • Glucocorticoids
  • Interleukin-1
  • Interleukin-1beta
  • RNA, Messenger
  • Dexamethasone