Inhibition of macrophage migration inhibitory factor reduces endometriotic implant size in mice with experimentally induced disease.

Journal of endometriosis Pub Date : 2011-09-30
Warren B Nothnick, Arlene Colvin, Kai Fan Cheng, Yousef Al-Abed
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Abstract

Endometriosis is a debilitating disease common in women of reproductive age characterized by pain and infertility. Macrophage migration inhibitory factor (MIF) is a cytokine whose expression is elevated in endometriotic tissue from women with the disease but the functional role of this factor in the pathogenesis of the disease is uncertain. To examine the role of MIF in the pathogenesis of endometriosis, we induced experimental disease in mice and examined the ability of the MIF antagonist, ISO-1, to reduce endometriotic implant size. Administration of ISO-1 resulted in a significant reduction in implant size and vascularity (as assessed by Flk1 mRNA expression) which was not associated with an alteration in the reproductive cycle. These data suggest that inhibition of MIF activity is associated with a significant reduction in endometriotic implant size and leads us to speculate that a similar approach of targeting MIF may prove useful in treating endometriosis in humans.

Abstract Image

抑制巨噬细胞迁移抑制因子可减少实验性诱导疾病小鼠子宫内膜异位症植入物的大小。
子宫内膜异位症是育龄妇女常见的一种衰弱性疾病,其特征是疼痛和不孕。巨噬细胞迁移抑制因子(MIF)是一种细胞因子,其表达在患有该疾病的女性子宫内膜异位症组织中升高,但该因子在该疾病发病机制中的功能作用尚不确定。为了研究MIF在子宫内膜异位症发病机制中的作用,我们在小鼠身上诱导了实验性疾病,并检测了MIF拮抗剂ISO-1减少子宫内膜异位症植入物大小的能力。给药ISO-1导致植入物大小和血管血管明显减少(通过Flk1 mRNA表达评估),这与生殖周期的改变无关。这些数据表明,抑制MIF活性与子宫内膜异位症植入物大小的显著减少有关,并使我们推测,针对MIF的类似方法可能被证明对治疗人类子宫内膜异位症有用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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