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Expression of monocyte chemoattractant protein 1 in human osteoblastic cells stimulated by proinflammatory mediators
Author(s) -
Zhu JianFu,
Valente Anthony J.,
Lorenzo Joseph A.,
Carnes David,
Graves Dana T.
Publication year - 1994
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650090721
Subject(s) - proinflammatory cytokine , monocyte , endocrinology , medicine , chemokine , tumor necrosis factor alpha , platelet derived growth factor , interleukin 8 , growth factor , chemistry , cytokine , biology , platelet derived growth factor receptor , inflammation , receptor
Monocyte chemoattractant protein 1 (MCP‐1) is a member of the chemokine superfamily of genes that induces chemotaxis of monocytes in inflammatory processes. The effects of interleukin‐1β (IL‐1β), tumor necrosis factor α (TNF‐α), interleukin‐6 (IL‐6), transforming growth factor β (TGF‐β), platelet‐derived growth factor (PDGF‐BB), parathyroid hormone (PTH), and 1,25(OH) 2 D 3 on MCP‐1 expression in human osteoblastic cells were compared. Inflammatory or proinflammatory cytokines stimulated the production of MCP‐1 in normal human osteoblastic cells as determined by RIA. The osteotrophic mediators PTH and 1,25(OH) 2 D 3 and PDGF‐BB had no effect on MCP‐1 expression. In further studies, the steady‐state mRNA and MCP‐1 protein levels in two human osteoblastic cell lines, MG‐63 and SaOS‐2, were examined. MCP‐1 expression at both the protein and mRNA levels was greatly increased by IL‐1β and TNF‐α. At the mRNA level, IL‐1β and TNF‐α strongly induced MCP‐1 expression; TGF‐β and IL‐6 induced MCP‐1 but to a lesser extent. No significant changes in MCP‐1 mRNA or MCP‐1 protein secretion were observed when cells were treated with PDGF‐BB, PTH, and 1,25(OH) 2 D 3 . When tested on preosteoclasts, MCP‐1 was shown to have no effect on the formation of multinucleated, tartrate‐resistant acid phosphatase (TRAP)‐positive osteoclastic cells.