TY - JOUR AB - Articular chondrocytes respond to extracellular influences by activating signaling pathways which change gene expression. One key signal transduction pathway of inflammatory joint disease is mediated by the p38MAPK which is known to be activated by the pro-inflammatory cytokine IL-1β. We used the p38MAPK inhibitor SB203580 and a whole human genome microarray in an in vitro inflammation model to identify genes regulated by this pathway in human chondrocytes. We found that 1,141 genes were regulated by IL-1β, and 646 genes were regulated by the inhibitor whereas 116 genes were co-regulated by both substances. To elucidate the overall effect of SB203580, a GoMiner pathway analysis was performed which revealed involvement of versatile biological processes. Predominantly affected terms were ‘response to stimulus’, ‘oxygen metabolism’ and ‘ligase activity’. We discuss herein the relevance and function of affected fields including the involved genes and unexpected effects of p38MAPK inhibition as it relates to the context of cartilage. Our results do not predict a pro-apoptotic or cancer promoting effect and markedly extend the knowledge on p38MAPK inhibition in chondrocytes beyond primary target genes. AD - Division for Biochemistry of Joint and Connective Tissue Diseases, Department of Orthopedics, University of Ulm, Ulm, Germany null AU - Joos,Helga AU - Albrecht,Wolfgang AU - Laufer,Stefan AU - Brenner,Rolf,E. DA - 2009/05/01 DO - 10.3892/ijmm_00000181 EP - 693 IS - 5 JO - Int J Mol Med PY - 2009 SN - 1107-3756 1791-244X SP - 685 ST - Influence of p38MAPK inhibition on IL-1β-stimulated human chondrocytes: A microarray approach T2 - International Journal of Molecular Medicine TI - Influence of p38MAPK inhibition on IL-1β-stimulated human chondrocytes: A microarray approach UR - https://doi.org/10.3892/ijmm_00000181 VL - 23 ER -