title: COMP does not directly modify the expression of genes involved in cartilage homeostasis in contrast to several other cartilage matrix proteins.
abstract: OBJECTIVE
  We investigated whether COMP may modify cartilage metabolism and play a role as an endogenous disease aggravating factor in OA.
  
  
  METHODS
  Full-length and momomeric COMP was recombinantly expressed in human embryonic kidney cells and purified it via affinity chromatography. Purified COMP was used to stimulate either primary human chondrocytes or cartilage explants. Changes in the expression profiles of inflammatory genes, differentiation markers and growth factors were examined by immunoassay and by quantitative real-time reverse-transcription polymerase chain reaction.
  
  
  RESULTS
  Incubation of primary human chondrocytes or cartilage explants in the presence of COMP did not induce statistically significant changes in the expression of IL-6, MMP1, MMP13, collagen I, collagen II, collagen X, TGF-β1 and BMP-2.
  
  
  CONCLUSIONS
  In contrast to collagen II and matrilin-3, COMP lacks the ability to trigger a proinflammatory response in chondrocytes, although it carries an RGD motif and can bind to integrins. COMP is a well-accepted biomarker for osteoarthritis but increased COMP levels do not necessarily correlate with inflammation.
authors.affiliation: Institute for Clinical Chemistry, University of Cologne , Cologne , Germany .
authors.forename: Johannes
authors.initials: J
authors.lastname: Ruthard
authors.forename: Matthias
authors.initials: M
authors.lastname: Kamper
authors.forename: Jörg H
authors.initials: JH
authors.lastname: Renno
authors.forename: Gertrud
authors.initials: G
authors.lastname: Kühn
authors.forename: Ute
authors.initials: U
authors.lastname: Hillebrand
authors.forename: Stefan
authors.initials: S
authors.lastname: Höllriegl
authors.forename: Wibke
authors.initials: W
authors.lastname: Johannis
authors.forename: Frank
authors.initials: F
authors.lastname: Zaucke
authors.forename: Andreas R
authors.initials: AR
authors.lastname: Klatt
mesh_terms: D000704:Analysis of Variance; D055396:Bone Morphogenetic Protein 2 / Q000378:metabolism; D002356:Cartilage / Q000378:metabolism / Q000502:physiology*; D064236:Cartilage Oligomeric Matrix Protein / Q000378:metabolism*; D002846:Chromatography, Affinity; D003094:Collagen / Q000378:metabolism; D017931:DNA Primers / Q000235:genetics; D005786:Gene Expression Regulation / Q000502:physiology*; D057809:HEK293 Cells; D006706:Homeostasis / Q000235:genetics / Q000502:physiology*; D006801:Humans; D007118:Immunoassay; D015151:Immunoblotting; D015850:Interleukin-6 / Q000378:metabolism; D020781:Matrix Metalloproteinase 1 / Q000378:metabolism; D053509:Matrix Metalloproteinase 13 / Q000378:metabolism; D010003:Osteoarthritis / Q000378:metabolism*; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: D055396:Bone Morphogenetic Protein 2; D064236:Cartilage Oligomeric Matrix Protein; D003094:Collagen; D017931:DNA Primers; D015850:Interleukin-6; D020781:Matrix Metalloproteinase 1; D053509:Matrix Metalloproteinase 13; D053773:Transforming Growth Factor beta1; C525718:BMP2 protein, human; C507079:MMP13 protein, human; C522360:MMP1 protein, human; C577553:TSP5 protein, human
keywords: COMP; TGF-β1; cartilage; cartilage explants; chondrocyte; matrilin; osteoarthritis