Interleukin-1beta increases RANTES gene expression and production in synovial fibroblasts from human temporomandibular joint

J Oral Pathol Med. 2004 Nov;33(10):629-33. doi: 10.1111/j.1600-0714.2004.00260.x.

Abstract

Background: Synovial fibroblasts of temporomandibular joint (TMJ) are poorly characterized, although they have important roles in progression of temporomandibular disorders (TMD). In this study, we investigated responses of synovial fibroblasts to interleukin (IL)-1beta.

Methods: We examined gene expression profiles of synovial fibroblasts in response to IL-1beta, using Affymetrix GeneChip. Regulated upon activation normal T-cell expressed and secreted (RANTES) gene expression was confirmed by polymerase chain reaction (PCR) and real-time PCR. RANTES protein levels were measured by enzyme-linked immunosorbent assay (ELISA).

Results: The RANTES was preferentially up-regulated in synovial fibroblasts by IL-1beta. The increase in RANTES gene expression in response to IL-1beta was confirmed by PCR and real-time PCR. Protein level of RANTES in synovial fibroblasts was also increased by IL-1beta.

Conclusions: The RANTES, a cc-type chemokine, has chemotactic effects on lymphocytes and monocytes. Increased gene expression and protein production of RANTES in synovial fibroblasts, in response to IL-1beta, may play an important role in recruitment of inflammatory cells into synovium and progression of synovitis in TMD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Chemokine CCL5 / biosynthesis*
  • Chemokine CCL5 / genetics
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Fibroblasts / metabolism
  • Gene Expression / drug effects*
  • Gene Expression Profiling
  • Humans
  • Interleukin-1 / pharmacology*
  • Oligonucleotide Array Sequence Analysis
  • Polymerase Chain Reaction / methods
  • RNA, Messenger / analysis
  • Synovial Membrane / cytology*
  • Synovial Membrane / metabolism*
  • Temporomandibular Joint / cytology
  • Temporomandibular Joint / metabolism*
  • Up-Regulation

Substances

  • Chemokine CCL5
  • Interleukin-1
  • RNA, Messenger