• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Molecular mechanisms involved in the estrogen-dependent regulation of calcineurin in systemic lupus erythematosus T cells.
【24h】

Molecular mechanisms involved in the estrogen-dependent regulation of calcineurin in systemic lupus erythematosus T cells.

机译：在系统性红斑狼疮T细胞中钙调神经磷酸酶的雌激素依赖性调节的分子机制。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Previous experiments in our laboratory indicated that calcineurin expression and PP2B phosphatase activity increased when estrogen was cultured with SLE T cells but not with T cells from normal women. In this report we extended our findings to show that estrogen receptor (ER) antagonism by ICI 182,780 inhibited the estrogen-dependent increase in calcineurin mRNA and phosphatase PP2B activity indicating that estrogen action was mediated through the ER. Inhibition of de novo protein synthesis with cycloheximide suggested that the estrogen-dependent increase in T cell calcineurin mRNA was a direct effect of the ER and new protein synthesis was not required. Estrogen increased calcineurin mRNA in systemic lupus erythematosus (SLE) T cells at 6 h after the start of culture correlating with increased phosphatase activity at this same time. Phosphatase activity increased significantly (P < 0.02) in lupus T cells cultured for 8 h in estradiol-containing medium. Reverse transcription and polymerase chain amplification revealed that ER-beta and ER-alpha were expressed in female and male T cells from SLE patients and normal controls. However, calcineurin steady-state mRNA levels were unaffected by estradiol in cultured T cells from male SLE patients and normal male and female controls. These data indicate that estrogen, bound to the ER, evokes a direct increase in calcineurin expression in T cells from female lupus patients. This gender-specific response suggests that ER function is altered in women with the female predominant autoimmune disease, SLE. Copyright 2000 Academic Press.
机译：我们实验室以前的实验表明，当雌激素与SLE T细胞一起培养而不与正常女性的T细胞一起培养时，钙调神经磷酸酶的表达和PP2B磷酸酶活性增加。在本报告中，我们扩展了研究结果，以显示ICI 182,780对雌激素受体（ER）的拮抗作用抑制了钙调神经磷酸酶mRNA和磷酸酶PP2B活性的雌激素依赖性增加，表明雌激素作用是通过ER介导的。用环己酰亚胺抑制从头合成蛋白质，表明T细胞钙调神经磷酸酶mRNA的雌激素依赖性增加是ER的直接作用，不需要新的蛋白质合成。在开始培养后6小时，雌激素增加了系统性红斑狼疮（SLE）T细胞中钙调神经磷酸酶的mRNA水平，这与同时增加的磷酸酶活性有关。在含雌二醇的培养基中培养8 h的狼疮T细胞的磷酸酶活性显着增加（P <0.02）。逆转录和聚合酶链扩增显示ER-beta和ER-alpha在SLE患者和正常对照组的女性和男性T细胞中表达。然而，钙调神经磷酸酶稳态mRNA水平不受男性SLE患者以及正常男性和女性对照的培养T细胞中雌二醇的影响。这些数据表明，与雌激素结合的雌激素引起女性狼疮患者T细胞钙调神经磷酸酶表达的直接增加。这种针对性别的反应表明，患有女性自身免疫性疾病（SLE）的女性的ER功能发生了改变。版权所有2000学术出版社。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号