Angiopoietin-1, angiopoietin-2 and Tie-2 expression in eutopic endometrium in advanced endometriosis

Angiopoietin-1, angiopoietin-2 and Tie-2 expression in eutopic endometrium in advanced endometriosis
复制标题

DOI:
10.1093/molehr/gal049
复制
发表时间:
2006-07-01
影响因子:
4
通讯作者:
Chung, Hye Won
Chung, Hye Won
中科院分区:
医学2区
文献类型:
--
作者:
Hur, Sung Eun;Lee, Ji Young;Chung, Hye Won

文献摘要

被引文献

相似文献

子宫内膜异位症是最常见的妇科疾病之一,但其病因和发病机制尚不清楚。子宫内膜异位症患者返流的月经残留物可能更容易通过细胞外蛋白分解和血管生成的作用在腹膜或卵巢内植入、侵袭和生长。已有研究认为,子宫内膜异位症患者的子宫内膜具有较高的血管生成活性,表达更多的血管生成因子。采用定量竞争聚合酶链式反应(QC-PCR法)结合反转录技术,检测56例重度子宫内膜异位症患者和非子宫内膜异位症患者卵泡和黄体周期在位内膜中血管生成素-1(Ang-1)、血管生成素-2(Ang-2)和Tie-2的表达。Western blotting分析在位内膜的蛋白表达。结果用Kruskal-Wallis和Mann-Whitney U检验进行统计学分析。子宫内膜异位症患者在位内膜Ang-1mRNA和蛋白表达水平高于正常子宫内膜(P<0.05),Ang-2mRNA表达水平高于正常子宫内膜(P&lt;0.05)。子宫内膜异位症患者在位内膜Tie-2mRNA和蛋白的表达与正常对照组无显著差异。这些结果提示,子宫内膜异位症患者在位内膜比非子宫内膜异位症患者在位内膜有更多的血管生成和生长,这是因为Ang-1mRNA和蛋白的表达以及Ang-2mRNA的表达高于非内异症患者的在位内膜。因此,血管生成活性增强可能是子宫内膜异位症的发病机制之一。
Endometriosis is one of the most common gynaecological disorders, but its aetiology and pathogenesis remain obscure. The refluxed menstrual debris in women with endometriosis may be more prone to implantation, invasion and growth in the peritoneum or ovary through the actions of extracellular proteolysis and angiogenesis. It has been hypothesized that the endometrium from women with endometriosis has higher angiogenic activity and expresses more angiogenic factors. Using quantitative competitive PCR (QC-PCR) combined with the reverse transcription of total RNA into cDNA, we investigated the expression of angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2) and Tie-2 in the eutopic endometrium from 56 women with severe endometriosis and that from 64 women without endometriosis during the follicular and luteal cycles. The protein expression from the eutopic endometrium was analysed by western blotting. Results were analysed statistically by Kruskal-Wallis and Mann-Whitney U tests. The eutopic endometrium from women with endometriosis expressed higher levels of mRNA and protein of Ang-1 (P < 0.05) and higher levels of mRNA of Ang-2 than the endometrium from normal women (P < 0.05). Tie-2 mRNA and protein expression from the eutopic endometrium did not differ significantly between endometriosis patients and normal controls. These results suggest that the eutopic endometrium from endometriosis patients is more angiogenic and prone to growth because of greater Ang-1 mRNA and protein expression and higher Ang-2 mRNA expression than the endometrium from women without endometriosis. Thus, increased angiogenic activity may be responsible for the pathogenesis of endometriosis.