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The article discusses the study which explores the connection between prostaglandin and osteoarthritis (OA) in human adult articular chondrocytes. The study measured cell survival, proliferation and total proteoglyean synthesis in alginate beads by reverse transcription-polymerase chain reaction (PCR) and Western blotting. The study represents effective therapeutic agents for the treatment of OA on human adult articular cartilage in vitro and receptor antagonist.

Pain-related neuropeptides released from synovial fibroblasts, such as substance P, have been implicated in joint destruction. Substance P-induced inflammatory processes are mediated via signaling through a G-protein-coupled receptor, that is, neurokinin-1 tachykinin receptor (NK1-R). We determined the pathophysiological link between substance P and its receptor in human adult articular cartilage homeostasis. We further examined if catabolic growth factors such as basic fibroblast growth factor (bFGF or FGF-2) or IL-1β accelerate matrix degradation via a neural pathway upregulation of substance P and NK1-R. We show here that substance P stimulates the production of cartilage-degrading enzymes, such as matrix metalloproteinase-13 (MMP-13), and suppresses proteoglycan deposition in human adult articular chondrocytes via NK1-R. Furthermore, we have demonstrated that substance P negates proteoglycan stimulation promoted by bone morphogenetic protein-7, suggesting the dual role of substance P as both a pro-catabolic and anti-anabolic mediator of cartilage homeostasis. We report that bFGF-mediated stimulation of substance P and its receptor NK1-R is, in part, through an IL-1β-dependent pathway. J. Cell. Physiol. 215: 452–463, 2008. © 2007 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]