title: Production of monocyte chemoattractant protein-1 by cultured glomerular epithelial cells: inhibition by dexamethasone.
abstract: Glomerular epithelial cells (GECs) have been shown to be one class of target cells in immunological and nonimmunological glomerular injury of glomerulonephritis, some cases of which are accompanied by infiltration of glomeruli by monocytes/macrophages. In this study we tested whether GECs in culture produce monocyte chemoattractant protein-1 (MCP-1), a potential molecule responsible for monocyte recruitment in inflammation, and whether the production is inhibited by glucocorticoid. GECs were obtained from outgrowth of rat glomeruli. Levels of MCP-1 mRNA and protein were determined by Northern blot analysis and ELISA, respectively. Northern blot analysis revealed the expression of MCP-1 mRNA in cytokine-treated GECs. The expression of MCP-1 mRNA was inhibited by dexamethasone. Quantitative analysis by ELISA confirmed the production of MCP-1 protein by GECs and the inhibitory effect of dexamethasone. These results indicate that cytokine-treated GECs produce and secrete MCP-1 and that the MCP-1 production is inhibited by dexamethasone. We suggest that MCP-1 produced by GECs may play a role in the recruitment of monocytes/macrophages in glomerulonephritis and that the therapeutic effect glucocorticoid on the disease might include the inhibition of the production of MCP-1.
authors.affiliation: Research Institute, International Medical Center of Japan, Tokyo, Japan. natoriya@imcj.go.jp
authors.forename: Y
authors.initials: Y
authors.lastname: Natori
authors.forename: Y
authors.initials: Y
authors.lastname: Natori
authors.forename: T
authors.initials: T
authors.lastname: Nishimura
authors.forename: H
authors.initials: H
authors.lastname: Yamabe
authors.forename: K
authors.initials: K
authors.lastname: Iyonaga
authors.forename: M
authors.initials: M
authors.lastname: Takeya
authors.forename: M
authors.initials: M
authors.lastname: Kawakami
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis* / Q000502:physiology; D002633:Chemotaxis / Q000187:drug effects; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D017077:Culture Media, Conditioned; D016207:Cytokines / Q000494:pharmacology*; D003907:Dexamethasone / Q000494:pharmacology*; D004797:Enzyme-Linked Immunosorbent Assay; D004847:Epithelial Cells; D004848:Epithelium / Q000187:drug effects / Q000276:immunology; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology; D007678:Kidney Glomerulus / Q000276:immunology*; D007963:Leukocytes, Mononuclear / Q000502:physiology; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D011994:Recombinant Proteins / Q000494:pharmacology; D014158:Transcription, Genetic / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D018932:Chemokine CCL2; D017077:Culture Media, Conditioned; D016207:Cytokines; D007375:Interleukin-1; D012333:RNA, Messenger; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D003907:Dexamethasone