Kovacs E J, Faunce D E, Ramer-Quinn D S, Mott F J, Dy P W, Frazier-Jessen M R
Department of Cell Biology, Loyola University, Maywood, IL, USA.
J Leukoc Biol. 1996 Apr;59(4):562-8. doi: 10.1002/jlb.59.4.562.
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.
我们最近证实,17β-雌二醇(E2)可抑制腹膜粘连形成。由于巨噬细胞在炎症和伤口愈合中起核心作用,我们选择研究E2是否能抑制JE(小鼠单核细胞趋化蛋白-1,即MCP-1)的表达。为实现此目的,将小鼠成纤维细胞与生理浓度的E2(3 - 300 pg/ml)一起培养,有无JE/MCP-1 mRNA表达诱导剂均可。未处理的细胞未能表达该信息,但刺激后,观察到JE/MCP-1 mRNA表达显著增加。在10 - 30 pg/ml时,E2对受刺激成纤维细胞中的JE/MCP-1 mRNA表达无影响。相反,较低和较高剂量的E2可抑制受刺激成纤维细胞中JE/MCP-1 mRNA的表达。用他莫昔芬处理可逆转E2对该信息表达的抑制作用。这些数据表明,JE/MCP-1 mRNA的表达部分受雌激素控制,并提示巨噬细胞募集可能受循环中E2水平的影响。