title: IL-1beta-induced expression of matrix metalloproteinases and gliostatin/platelet-derived endothelial cell growth factor (GLS/PD-ECGF) in a chondrosarcoma cell line (OUMS-27).
abstract: The purpose of this study was to examine how chondrocytes are involved in the molecular mechanism of inflammation in rheumatoid arthritis (RA). A chondrosarcoma cell line (OUMS-27) was cultured and treated with interleukin-1beta (IL-1beta). Changes in the expression levels of matrix metalloproteinase-1 (MMP-1), metalloproteinase-13 (MMP-13), and gliostatin/platelet-derived endothelial cell growth factor (GLS/PD-ECGF) were assessed by reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assays. IL-1beta induced the expressions of MMP-1, MMP-13, and GLS mRNAs and proteins in a dose-dependent manner. Selective inhibition of the p38 mitogen-activated protein kinase (p38 MAPK) pathway with SB 203580 and SB 202190 blocked the expression of MMP-1, MMP-13, and GLS more strongly than selective in hibition of the extracellular signal-regulated kinase 1 and 2 (ERK1/2) pathway by PD 98059. These findings suggest that chondrocytes may intensify cartilage destruction and inflammation in RA by the induction of MMP-1, MMP-13, and GLS by IL-1beta and that the p38 MAPK pathway plays an important role in these inductions.
authors.affiliation: Department of Orthopedic Surgery, Nagoya City University Medical School, Japan. ieda@sunprom.med.nagoya-cu.ac.jp
authors.forename: Y
authors.initials: Y
authors.lastname: Ieda
authors.forename: Y
authors.initials: Y
authors.lastname: Waguri-Nagaya
authors.forename: T
authors.initials: T
authors.lastname: Iwahasi
authors.forename: T
authors.initials: T
authors.lastname: Otsuka
authors.forename: N
authors.initials: N
authors.lastname: Matsui
authors.forename: M
authors.initials: M
authors.lastname: Namba
authors.forename: K
authors.initials: K
authors.lastname: Asai
authors.forename: T
authors.initials: T
authors.lastname: Kato
mesh_terms: D001483:Base Sequence; D002813:Chondrosarcoma / Q000473:pathology / Q000503:physiopathology; D017364:Collagenases / Q000187:drug effects / Q000235:genetics*; D004305:Dose-Response Relationship, Drug; D004797:Enzyme-Linked Immunosorbent Assay; D015870:Gene Expression / Q000502:physiology; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism* / Q000494:pharmacology; D020781:Matrix Metalloproteinase 1 / Q000187:drug effects / Q000235:genetics*; D053509:Matrix Metalloproteinase 13; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D008969:Molecular Sequence Data; D012333:RNA, Messenger / Q000032:analysis; D012016:Reference Values; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012680:Sensitivity and Specificity; D013939:Thymidine Phosphorylase / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism; D014407:Tumor Cells, Cultured; D048051:p38 Mitogen-Activated Protein Kinases
chemical_list: D007375:Interleukin-1; D012333:RNA, Messenger; D013939:Thymidine Phosphorylase; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D017364:Collagenases; C507079:MMP13 protein, human; D053509:Matrix Metalloproteinase 13; D020781:Matrix Metalloproteinase 1