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Increased proteolysis in endometriotic tissue and endometrium in women who develop endometriosis may facilitate invasion

机译:在开发子宫内膜异位症的女性内膜静脉肌组织和子宫内膜中增加的蛋白质溶解可能促进入侵

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The pathogenesis of endometiiosls is presumed to be related to adhesion and invasion in ectopic sites of dispersed shed endometrium. The mechanism is poorly understood The aim of this project was to investigate the role of the plasminogen-activating system (PAs), including urokinase plasminogen activator (uPA), urokinase plasminogen activator receptor (uPAR), and plasminogen activator inhibitor-1 (PAI-1), in the pathogenesis of endometriosis The system is involved in tissue degradation and remodelling under both normal and pathological conditions This project included the assay of the three proteins in tissue homogenates, localisation of both the proteins and their mRNA in tissue sections, and studies of their release in cell cultures Our major findings were an up-regulation of mRNA for all three factors and higher concentrations of uPA, and PAI-1 in endometriotic and endometrial tissue from women with endometriosis compared to control endometiium,. These findings might be of importance for menstrual shedding, adhesion, and invasion of viable endometrial fragments. The studies have shown above all that there is an important difference in the expression of the components of the PAs in endometrium from women with endometriosis compared to healthy endometrium, supporting the hypothesis that ectopic endometrial invasion takes place, at least partly, as a consequence of a disturbed fibrinolytic activity in the eutopic endometrium.
机译:endometiiosls的发病机制被假定在分散棚子宫内膜异位网站进行相关黏附和侵袭。该机制知之甚少该项目的目的是调查纤溶酶原活化系统(PAS),包括尿激酶型纤溶酶原激活剂(uPA),尿激酶纤溶酶原激活物受体(uPAR)和纤溶酶原激活物抑制剂-1(的作用PAI- 1),在子宫内膜异位症的系统参与组织退化和正常和病理条件下重塑的发病机理该项目包括了三种蛋白质在组织匀浆中的蛋白质都和他们的组织切片的mRNA,并研究分析,国产化它们在细胞培养中释放我们的主要发现与对照组相比endometiium是mRNA的所有三个因素在子宫内膜异位和子宫内膜组织的上调和uPA的浓度较高,而PAI-1子宫内膜异位症,。这些发现可能是月经脱落,附着力强,可行子宫内膜碎片侵入重要性。该研究显示,超过一切存在来自子宫内膜异位症与健康子宫内膜PA的组分的表达一个重要的区别,支持异位内膜侵入发生,至少部分地,假设作为的后果一个在在位内膜扰乱纤溶活性。

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