PMID- 1624809 OWN - NLM STAT- MEDLINE DCOM- 19920811 LR - 20220227 IS - 0022-1767 (Print) IS - 0022-1767 (Linking) VI - 149 IP - 2 DP - 1992 Jul 15 TI - Production of monocyte chemoattractant protein-1 by inflamed synovial tissue and cultured synoviocytes. PG - 722-7 AB - This study analyzes the expression of monocyte chemoattractant protein-1 (MCP-1) by inflamed synovial tissue and defines its regulation in cultured synoviocytes. Synoviocytes from patients with rheumatoid arthritis and osteoarthritis express the 0.7-kb MCP-1 mRNA. Stimulation of synoviocytes with IL-1, TNF-alpha, LPS, platelet-derived growth factor, and transforming growth factor-beta-1, but not with basic fibroblast growth factor causes a marked increase in MCP-1 mRNA levels. Expression of the MCP-1 gene is inducible by activators of the protein kinase A (cAMP) and C (PMA) signal transduction pathways and is differentially regulated by the steroids dexamethasone and retinoic acid. Cultured synoviocytes de novo synthesize 12-, 15-, and 15.2-kDa MCP-1 proteins, which increase after stimulation with IL-1. Synovial tissues from donors without joint disease and from patients with rheumatoid or osteoarthritis were analyzed for MCP-1 mRNA expression by in situ hybridization. In these samples MCP-1 mRNA expressing cells were predominantly found in the sublining cell layers, whereas specimens of normal synovial tissue contained only few positive cells. These results identify synoviocytes as a source of MCP-1. Its expression is controlled by peptide regulatory factors that are known to be present in arthritic joints. Detection of cells producing MCP-1 mRNA in synovial tissues from patients with arthritis shows that this gene is expressed in vivo and suggests that MCP-1 can play a role in recruiting monocytes in joint inflammation. FAU - Villiger, P M AU - Villiger PM AD - Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, La Jolla 92093. FAU - Terkeltaub, R AU - Terkeltaub R FAU - Lotz, M AU - Lotz M LA - eng GR - AG-07996/AG/NIA NIH HHS/United States GR - AR-39799/AR/NIAMS NIH HHS/United States GR - DK-36702/DK/NIDDK NIH HHS/United States PT - Journal Article PT - Research Support, U.S. Gov't, Non-P.H.S. PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - J Immunol JT - Journal of immunology (Baltimore, Md. : 1950) JID - 2985117R RN - 0 (Chemokine CCL2) RN - 0 (Chemotactic Factors) RN - 0 (Cytokines) RN - 0 (Glucocorticoids) RN - 0 (Growth Substances) RN - 0 (RNA, Messenger) SB - IM MH - Base Sequence MH - Cells, Cultured MH - Chemokine CCL2 MH - Chemotactic Factors/*biosynthesis/genetics MH - Cytokines/pharmacology MH - Gene Expression Regulation MH - Glucocorticoids/pharmacology MH - Growth Substances/pharmacology MH - Humans MH - Molecular Sequence Data MH - RNA, Messenger/analysis MH - Synovial Membrane/*metabolism MH - Synovitis/*metabolism EDAT- 1992/07/15 00:00 MHDA- 1992/07/15 00:01 CRDT- 1992/07/15 00:00 PHST- 1992/07/15 00:00 [pubmed] PHST- 1992/07/15 00:01 [medline] PHST- 1992/07/15 00:00 [entrez] PST - ppublish SO - J Immunol. 1992 Jul 15;149(2):722-7.