Estrogen regulation of JE/MCP-1 mRNA expression in fibroblasts

We have recently demonstrated that 17β‐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). T...

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Veröffentlicht in:Journal of leukocyte biology 1996-04, Vol.59 (4), p.562-568
Hauptverfasser: Kovacs, E. J., Faunce, D. E., Ramer‐Quinn, D. S., Mott, F. J., Dy, P. ‐W. W., Frazier‐Jessen, M. R.
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Sprache:eng
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Zusammenfassung:We have recently demonstrated that 17β‐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.
ISSN:0741-5400
1938-3673
DOI:10.1002/jlb.59.4.562