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J Leukoc Biol ; 59(4): 562-8, 1996 Apr.
Article in English | MEDLINE | ID: mdl-8613705

ABSTRACT

We have recently demonstrated that 17 beta-estradiol (E2) inhibits peritoneal adhesion formation. Because macrophages play a central role in inflammation and wound healing, we chose to investigate whether the E2 could inhibit the expression of JE, the murine monocyte chemoattractant protein-1 (MCP-1). To accomplish this, murine fibroblasts were cultured with physiological concentrations of E2 (3-300 pg/ml) with or without inducers of JE/MCP-1 mRNA expression. Untreated cells failed to express the message, but, following stimulation, a marked increase in JE/MCP-1 mRNA expression was observed. At 10-30 pg/ml, E2 had no effect on JE/MCP-1 mRNA expression in stimulated fibroblasts. In contrast, lower and higher doses of E2 inhibited the expression of JE/MCP-1 mRNA in stimulated fibroblasts. Treatment with tamoxifen reversed the E2-inhibition of expression of the message. These data demonstrate that JE/MCP-1 mRNA expression is controlled, in part, by estrogen and suggest that macrophage recruitment may be affected by circulating levels of E2.


Subject(s)
Chemokine CCL2/biosynthesis , Estradiol/pharmacology , Fibroblasts/drug effects , Fibroblasts/metabolism , RNA, Messenger/metabolism , 3T3 Cells/drug effects , 3T3 Cells/metabolism , 3T3 Cells/physiology , Animals , Cells, Cultured , Chemokine CCL2/genetics , Dexamethasone/pharmacology , Estrogen Antagonists/pharmacology , Fibroblasts/physiology , Gene Expression Regulation/drug effects , Humans , Mice , Platelet-Derived Growth Factor/antagonists & inhibitors , Platelet-Derived Growth Factor/pharmacology , RNA, Messenger/genetics , Sensitivity and Specificity , Tamoxifen/pharmacology
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