High temperature requirement A1, transforming growth factor beta1, phosphoSmad2 and Ki67 in eutopic and ectopic endometrium of women with endometriosis

Abstract

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.

Endometrium metabolomic profiling reveals potential biomarkers for diagnosis of endometriosis at minimal-mild stages

“…According to the widely accepted theory of retrograde menstruation, the endometrium is the source of ectopic endometriotic foci. Previous studies showed that the eutopic endometrium contributed to the pathogenesis of endometriosis due to the increase of proliferation, migration and invasion of ectopic endometrium [29][30][31][32][33]. In this study, we did not detect a significant difference in patients' uric acid level in serum.…”

Different macrophages equally induce EMT in endometria of adenomyosis and normal

“…The protein expression levels of TGFB1 and SMAD3 between eutopic and normal endometrium groups differed insignificantly, which is inconsistent with previous studies (Johnson et al 2005, Cruz et al 2015. Another research reported that only weak upregulation of TGFB1 in endometriosis eutopic endometrium occurred compared with the controls (Goteri et al 2015). The present study is the first to compare the protein expression levels of TGFB1 and Figure 7 (A) Representative photomicrographs of macrophages with and without co-culturing (original magnification, ×400).…”

Integrated analysis of long non-coding RNA and mRNA expression in endometrial stromal cells induced by poly (I:C) identifies immune response genes

“…Retinol dehydrogenase 10 (RDH10) is a key enzyme for vitamin A metabolism and is essential for embryonic patterning, morphogenesis and survival [30]. In addition, TGF-β1 (transforming growth factor-beta 1) is abundantly expressed in the endometrium and secreted into the uterine fluid to regulate uterine function [31]. Growth and differentiation factor 9 (GDF9) is secreted by oocytes and plays a leading role in the control of ovarian function in reproduction [32].…”