High temperature requirement A1, transforming growth factor beta1, phosphoSmad2 and Ki67 in eutopic and ectopic endometrium of women with endometriosis.
High temperature requirement A1, transforming growth factor beta1, phosphoSmad2 and Ki67 in eutopic and ectopic endometrium of women with endometriosis.
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DOI：
10.4081/ejh.2015.2570
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发表时间：
2015-12-09
期刊：
影响因子：
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通讯作者：
Marzioni D
中科院分区：
文献类型：
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作者：
Goteri G;Altobelli E;Tossetta G;Zizzi A;Avellini C;Licini C;Lorenzi T;Castellucci M;Ciavattini A;Marzioni D
越来越多的证据支持这一假说，即TGFβ1信号可能是由高温需要A1（HtrA 1）丝氨酸蛋白酶介导的，作用于重要的调节机制，如细胞增殖和迁移。现在越来越多的证据表明，HtrA 1参与了几种病理的发展和进展。本研究的目的是评估：i）子宫内膜异位症患者在位和异位子宫内膜中HtrA 1和TGFβ1的表达是否不同; ii）HtrA 1是否与TGFβ1、pSmad和Ki 67相关。本研究包括10例卵巢子宫内膜异位症患者（病例组）和10例非子宫内膜异位症患者（对照组）。对子宫内膜组织进行HtrA 1、TGFβ1、pSmad和Ki 67分子的免疫组化H评分分析。通过非参数Kruskal-Wallis检验进行数据评价，并应用斯皮尔曼相关性来评价上皮和基质室中研究的分子之间的关系。子宫内膜异位症患者异位内膜和在位内膜上皮细胞中HtrA 1的表达明显低于对照组。TGFβ 1在在位内膜上皮和间质区表达明显增高，而在异位内膜上皮和间质区表达明显降低。此外，与对照组相比，Ki 67显著增加，并且在在位和异位子宫内膜中检测到pSMAd 2的增加，但不显著。总之，TGFβ1和pSmad 2之间以及HtrA 1和TGFβ1之间的显著直接相关性以及在位子宫内膜间质区室中非常显著的Ki 67增加提示HtrA 1可能参与子宫内膜异位症的发病机制。
Increasing evidence supports the hypothesis that TGFβ1 signalling may be mediated by high temperature requirement A1 (HtrA1) serine protease, acting on important regulatory mechanisms such as cell proliferation and mobility. Evidence is now accumulating to suggest that HtrA1 is involved in the development and progression of several pathologies. The aim of this study was to evaluate: i) if HtrA1 and TGFβ1 expressions differ in eutopic and ectopic endometrium in women with endometriosis; ii) if HtrA1 correlates to TGFβ1, pSmad and Ki67. This study was carried out including 10 women with ovarian endometriosis (cases) and 10 women with non endometriotic diseases (controls). Endometrial tissue underwent immunohistochemical H-score analysis for HtrA1, TGFβ1, pSmad and Ki67 molecules. Data evaluation was performed by a nonparametric Kruskal-Wallis test and Spearman correlation was applied to evaluate the relationship among the molecules investigated in the epithelial and in the stromal compartment. The HtrA1 was significantly decreased in ectopic and eutopic endometrium of women with endometriosis when compared with control endometrium in epithelial compartment. TGFβ1was significantly increased in eutopic endometrium and decreased in ectopic endometrium in epithelial and stromal compartment. In addition, Ki67 was significantly increased and an increase, but not significant, was detected for pSMAd2 in eutopic and ectopic endometrium compared to control one. In summary, the significant direct correlation between TGFβ1 and pSmad2 as well as between HtrA1 and TGFβ1 and the very significant increase of Ki67 in stromal compartment of eutopic endometrium suggest a possible involvement of HtrA1 in the pathogenesis of endometriosis.