title: The infrapatellar fat pad induces inflammatory and degradative effects in articular cells but not through leptin or adiponectin.
abstract: OBJECTIVE
  Based on a novel approach suggesting a role of adipose tissue in osteoarthritis (OA), we aimed to determine whether the infrapatellar fat pad (IFP) may affect joint cell functions through adipokines.
  
  
  METHODS
  The conditioned media of IFP and subcutaneous adipose tissue from OA patients were used to determine the production of leptin and adiponectin, and to stimulate chondrocytes and fibroblast-like synoviocytes (FLS). Blocking experiments were carried out to evaluate the contribution of adipokines to IFP effects. The gene expression of inflammatory and degradative proteins, growth factors and components of the extracellular matrix, and the production of inflammatory mediators and metalloproteases were determined to evaluate cell response to fat-conditioned media.
  
  
  RESULTS
  IFP releases elevated amounts of leptin and adiponectin independently of the body mass index and the gender. The conditioned media from IFP strongly induce the expression of inflammatory genes in both articular cells and the expression of degradative genes in chondrocytes, but remain ineffective in regulating the expression of aggrecan, type 2 collagen or growth factors. Blocking leptin or adiponectin does not change the cell response to IFP. A great variability between patients is found when compared the inflammatory activity of paired samples of IFP and subcutaneous adipose tissue.
  
  
  CONCLUSIONS
  IFP may trigger both cartilage destruction and inflammation of the synovium, but not through leptin or adiponectin. The data suggest also that IFP may have specific inflammatory phenotypic features independent from the general phenotype found in obesity.
authors.affiliation: UMR 7365 CNRS-Université de Lorraine, Faculté de Medecine, Vandoeuvre-les-Nancy, France.
authors.forename: Jean-Baptiste
authors.initials: JB
authors.lastname: Gross
authors.affiliation: UMR 7365 CNRS-Université de Lorraine, Faculté de Medecine, Vandoeuvre-les-Nancy, France.
authors.forename: Cecile
authors.initials: C
authors.lastname: Guillaume
authors.affiliation: UMR 7365 CNRS-Université de Lorraine, Faculté de Medecine, Vandoeuvre-les-Nancy, France.
authors.forename: Pascale
authors.initials: P
authors.lastname: Gegout-Pottie
authors.affiliation: UMR 7365 CNRS-Université de Lorraine, Faculté de Medecine, Vandoeuvre-les-Nancy, France.
authors.forename: Pascal
authors.initials: P
authors.lastname: Reboul
authors.affiliation: UMR 7365 CNRS-Université de Lorraine, Faculté de Medecine, Vandoeuvre-les-Nancy, France.
authors.forename: Jean-Yves
authors.initials: JY
authors.lastname: Jouzeau
authors.affiliation: UMR 7365 CNRS-Université de Lorraine, Faculté de Medecine, Vandoeuvre-les-Nancy, France.
authors.forename: Didier
authors.initials: D
authors.lastname: Mainard
authors.affiliation: UMR 7365 CNRS-Université de Lorraine, Faculté de Medecine, Vandoeuvre-les-Nancy, France. nathalie.presle@univ-lorraine.fr.
authors.forename: Nathalie
authors.initials: N
authors.lastname: Presle
mesh_terms: D052242:Adiponectin / Q000378:metabolism*; D000273:Adipose Tissue / Q000378:metabolism* / Q000473:pathology; D000368:Aged; D000369:Aged, 80 and over; D002358:Cartilage, Articular / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D019902:Chondrocytes / Q000378:metabolism / Q000473:pathology; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000378:metabolism* / Q000473:pathology; D007719:Knee Joint / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D020738:Leptin / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D020370:Osteoarthritis, Knee / Q000378:metabolism* / Q000473:pathology / Q000601:surgery
chemical_list: D052242:Adiponectin; D016207:Cytokines; D020738:Leptin