title: Monoclonal expansion of synoviocytes in rheumatoid arthritis.
abstract: OBJECTIVE
  To examine whether synoviocytes from patients with rheumatoid arthritis (RA) have a stronger growth ability than those from patients with osteoarthritis (OA), and to determine whether these synoviocytes clonally expand in situ.
  
  
  METHODS
  Synovial tissues from 13 RA patients and 4 OA patients were cultured, and their ability to form colonies in soft agarose was examined. RA and OA synoviocytes were also examined in varying concentrations of fetal calf serum (FCS)-containing medium to test the effects of FCS on colony formation. DNA was extracted from clones with colony-forming ability in nonpannus lesions and from synoviocytes in pannus lesions. Restriction fragment length polymorphism (RFLP) analysis was used to examine phosphoglycerate kinase 1 (PGK-1) gene patterns. Production of cytokines by these cells was also assessed.
  
  
  RESULTS
  All 13 RA synoviocytes exhibited colony formation, whereas none of the 4 OA synoviocytes did. This tendency was also seen with all of the concentrations of FCS examined, although growth varied in a dose-dependent manner. In contrast to OA synovial clones, cloned RA synoviocytes obtained from colonies exhibited a partial RFLP PGK-1 gene pattern, suggesting that the clones originated from monoclonal cells. Of note, 3 of 7 noncloned synoviocytes from pannus lesions exhibited a monoclonal pattern. Pannus cells produced high levels of transforming growth factor beta and platelet-derived growth factor.
  
  
  CONCLUSIONS
  These findings suggest that synoviocytes with a strong growth ability are present in the rheumatoid synovium, and that these cells expand monoclonally, particularly in pannus lesions.
authors.affiliation: St. Marianna University School of Medicine, Kawasaki, Japan.
authors.forename: F
authors.initials: F
authors.lastname: Imamura
authors.forename: H
authors.initials: H
authors.lastname: Aono
authors.forename: T
authors.initials: T
authors.lastname: Hasunuma
authors.forename: T
authors.initials: T
authors.lastname: Sumida
authors.forename: H
authors.initials: H
authors.lastname: Tateishi
authors.forename: S
authors.initials: S
authors.lastname: Maruo
authors.forename: K
authors.initials: K
authors.lastname: Nishioka
mesh_terms: D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D002356:Cartilage / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D002455:Cell Division / Q000502:physiology; D002999:Clone Cells; D015971:Gene Expression Regulation, Enzymologic / Q000276:immunology; D006801:Humans; D006965:Hyperplasia; D008297:Male; D008875:Middle Aged; D010003:Osteoarthritis / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D010735:Phosphoglycerate Kinase / Q000235:genetics; D010982:Platelet-Derived Growth Factor / Q000276:immunology / Q000378:metabolism; D012150:Polymorphism, Restriction Fragment Length; D013234:Stem Cells / Q000166:cytology; D013583:Synovial Membrane / Q000166:cytology* / Q000201:enzymology / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000276:immunology / Q000378:metabolism
chemical_list: D010982:Platelet-Derived Growth Factor; D016212:Transforming Growth Factor beta; D010735:Phosphoglycerate Kinase