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Tumor necrosis factor‐ α increases chemokine gene expression and production in synovial fibroblasts from human temporomandibular joint
Author(s) -
Ogura Naomi,
Tobe Makiko,
Sakamaki Hiroyuki,
Nagura Hideaki,
Abiko Yoshimitsu,
Kondoh Toshirou
Publication year - 2005
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.2005.00302.x
Subject(s) - chemokine , synovitis , tumor necrosis factor alpha , synovial membrane , cancer research , monocyte , immunology , macrophage inflammatory protein , cytokine , inflammation , medicine , pathology , biology , arthritis
Background: Synovitis, which is characterized by infiltration of inflammatory cells, often accompanies progression of clinical symptoms of the temporomandibular joint (TMJ). Synovial fibroblasts of the TMJ are believed to play important roles in progression of synovitis. The purpose of this study was to examine production and gene expression of chemokines by synovial fibroblasts stimulated by tumor necrosis factor‐ α (TNF‐ α ). Methods: Protein levels of chemokines were measured by enzyme‐linked immunosorbent assay (ELISA). Gene expression of chemokines was analyzed by real‐time polymerase chain reaction (PCR). Results: Production of interleukin (IL)‐8, growth‐related oncogene (GRO)‐ α , monocyte chemoattractant protein (MCP)‐1, and regulated upon activation normal T‐cell expressed and secreted (RANTES) protein by synovial fibroblasts was increased by TNF‐ α . In contrast, stromal cell‐derived factor (SDF)‐1 α , macrophage inflammatory protein (MIP)‐1 α and ‐1 β were not detectable in conditioned media of synovial fibroblasts, with or without TNF‐ α treatment. Increases in gene expression of IL‐8, GRO‐ α , MCP‐1, and RANTES in response to TNF‐ α treatment were detected. Conclusions: Increased protein production and gene expression of chemokines by synovial fibroblasts in response to TNF‐ α treatment appears to play an important role in recruitment of inflammatory cells into synovium and the progression of synovitis in the TMJ.