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J Leukoc Biol ; 59(4): 562-8, 1996 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-8613705

RESUMO

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.


Assuntos
Quimiocina CCL2/biossíntese , Estradiol/farmacologia , Fibroblastos/efeitos dos fármacos , Fibroblastos/metabolismo , RNA Mensageiro/metabolismo , Células 3T3/efeitos dos fármacos , Células 3T3/metabolismo , Células 3T3/fisiologia , Animais , Células Cultivadas , Quimiocina CCL2/genética , Dexametasona/farmacologia , Antagonistas de Estrogênios/farmacologia , Fibroblastos/fisiologia , Regulação da Expressão Gênica/efeitos dos fármacos , Humanos , Camundongos , Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores , Fator de Crescimento Derivado de Plaquetas/farmacologia , RNA Mensageiro/genética , Sensibilidade e Especificidade , Tamoxifeno/farmacologia
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