The Role of Placental Protein 14 in the Pathogenesis of Endometriosis

Wang, Ping; Zhu, Libo; Zhang, Xinmei

doi:10.1177/1933719113488452

Cited by 7 publications

(4 citation statements)

References 29 publications

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“…29 Glycodelin-A has also been proposed as a potential biomarker of endometriosis; indeed several studies reported an increase in GdA concentration in serum and peritoneal fluid of women affected by this pathology. 7,18,30 Moreover, by both immunohistochemistry and microarray analysis, it has been reported a decrease in GdA expression at the window of implantation in eutopic versus healthy endometrium. 5,19 Our results are partially in agreement with these papers since we could confirm, by 2-D electrophoresis and immunofluorescence analysis, a decrease in GdA expression at the window of implantation in eutopic compared to healthy endometrium.…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of GdA Expression in Endometrium of Women With Endometriosis: Implication for Endometrial Receptivity

et al. 2018

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Glycodelin-A (GdA) has been proposed to represent a potential biomarker of endometrial function, but little is known about its expression during the different phases of the menstrual cycle and under pathological conditions. In the light of its potential importance also in embryo implantation, we aimed to evaluate the expression profile of GdA as well as the presence of different glycosylated glycoforms and the immunolocalization in endometrial tissue from women with endometriosis and in women with proven fertility, at different times during the menstrual cycle. Our results showed that GdA is synthesized by endometrial epithelial and stromal cells, both in healthy endometrium and eutopic endometrium from women with endometriosis, with a profile including several glycosylated glycoforms, differentially expressed in each phase of the menstrual cycle. During the secretory phase, a significant increase in GdA protein expression, with a different glycoforms profile, was observed in endometriotic eutopic endometrium. Protein localization in eutopic endometrial tissue resulted significantly different in comparison with endometrium from women with proven fertility. This study indicate that GdA is a complex glycoprotein including up to 6 different glycoforms specifically expressed during the different phase of the menstrual cycle; in pathologic conditions such as endometriosis, the expression profile is altered possibly related to the impaired endometrial receptivity.

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Section: Discussionmentioning

confidence: 99%

Dysregulation of GdA Expression in Endometrium of Women With Endometriosis: Implication for Endometrial Receptivity

et al. 2018

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“…The level of FOXA2 protein decreases substantially in the ectopic tissue from patients with endometriosis relative to normal endometrium, which corresponds with the results reported for placenta protein (PP-14) from serum of patients with endometriosis. 51 The staining also reveals that FOXA2 is mainly present in the nucleus of both endometrial glandular and luminal epithelial cells but not in stroma cells. These results confirmed our integrative analysis results, suggesting that FOXA2 and TFAP2C might be implicated in endometriosis.…”

Section: Validation Of Foxa2 and Tfap2c Downregulation In Endometriosismentioning

confidence: 95%

Integrative Analysis Reveals Regulatory Programs in Endometriosis

et al. 2015

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Endometriosis is a common gynecological disease found in approximately 10% of reproductive-age women. Gene expression analysis has been performed to explore alterations in gene expression associated with endometriosis; however, the underlying transcription factors (TFs) governing such expression changes have not been investigated in a systematic way. In this study, we propose a method to integrate gene expression with TF binding data and protein-protein interactions to construct an integrated regulatory network (IRN) for endometriosis. The IRN has shown that the most regulated gene in endometriosis is RUNX1, which is targeted by 14 of 26 TFs also involved in endometriosis. Using 2 published cohorts, GSE7305 (Hover, n = 20) and GSE7307 (Roth, n = 36) from the Gene Expression Omnibus database, we identified a network of TFs, which bind to target genes that are differentially expressed in endometriosis. Enrichment analysis based on the hypergeometric distribution allowed us to predict the TFs involved in endometriosis (n = 40). This included known TFs such as androgen receptor (AR) and critical factors in the pathology of endometriosis, estrogen receptor α, and estrogen receptor β. We also identified several new ones from which we selected FOXA2 and TFAP2C, and their regulation was confirmed by quantitative real-time polymerase chain reaction and immunohistochemistry (IHC). Further, our analysis revealed that the function of AR and p53 in endometriosis is regulated by posttranscriptional changes and not by differential gene expression. Our integrative analysis provides new insights into the regulatory programs involved in endometriosis.

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“…Gd-A suppresses the function of T cells and/or NK cells by its direct anti-proliferative and/or pro-apoptotic action on these immune cells [ 29 – 31 , 40 , 41 ]. It has been reported that endometriosis patients had significantly higher serum and peritoneal fluid (PF) concentrations of Gd-A compared with control women without endometriosis and displayed Gd-A expression in endometriosis lesions [ 43 , 44 ]. All these findings indicate that Gd-A exhibits a potential role in creating an immunosuppressive environment in pelvis and in the pathogenesis of endometriosis.…”

Section: Discussionmentioning

confidence: 99%

Is neonatal uterine bleeding responsible for early-onset endometriosis?

Ogawa

Khan

Kuroboshi

et al. 2023

Reprod Biol Endocrinol

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Background It has been hypothesized that the origin of early-onset endometriosis could be from endometrial mesenchymal stem cells (eMSCs) in neonatal uterine blood (NUB). There is no information on the possible mechanistic basis linking an association between NUB/neonatal endometrium and development of early-onset endometriosis. In this study we performed a series of experiments to clarify the mechanistic link between NUB and/or neonatal endometrium and development of early-onset endometriosis. Methods We retrospectively collected postmortem neonatal endometria (n = 15) and prospectively collected NUB (n = 18) of female babies for the analysis of different biological markers including eMSCs. Immunohistochemical analysis of neonatal endometria was performed to examine the expression patterns of ovarian steroid receptors (ER/PGR), decidualization (prolactin, IGFBP1), pre-decidualization (Glycodelin A, α-SMA), proliferation (Ki-67 index), vascularity (CD31 + cells), immunocompetent CD68+, CD45+, CD56 + cells and some putative markers of eMSCs. Cell transfer method and immunocytochemistry were used to investigate the eMSCs and/or endometrial cells in NUB. Results Immunohistochemical analysis of postmortem neonatal endometria revealed variable staining response to ER/PGR, decidual markers, and substantial proliferative and angiogenic activity. A moderate to strong immunoexpression of Glycodelin-A was found in both neonatal and adult endometria. The tissue infiltration of CD56+, CD45 + and CD68 + immunocompetent cells was significantly low in neonatal endometria than that in adult endometria (p = 0.0003, p < 0.0001, p = 0.034, respectively). No eMSCs or even endometrial cells were detected in NUB. However, a variable expression of some phenotypes of eMSCs (CD90/CD105) was found in neonatal endometria. Conclusions Based on our serial experiments we did not find any supporting evidence for the role of NUB in early-onset endometriosis. Neonatal endometria showed variable expression of ovarian steroid receptors, decidualization, and a substantial amount of proliferative and angiogenic activity. As an alternative mechanism, a significantly less tissue accumulation of immunocompetent cells in neonatal endometria may explain the survival of ER + and PGR + cells should they make entry into the pelvis and consequent development of early endometriosis with the onset of ovarian function. Future study with large sample size and application of modified technological tools is warranted to test the NUB hypothesis and to clarify their biological or clinical significance. Trial registration not applicable.

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The Role of Placental Protein 14 in the Pathogenesis of Endometriosis

Cited by 7 publications

References 29 publications

Dysregulation of GdA Expression in Endometrium of Women With Endometriosis: Implication for Endometrial Receptivity

Dysregulation of GdA Expression in Endometrium of Women With Endometriosis: Implication for Endometrial Receptivity

Integrative Analysis Reveals Regulatory Programs in Endometriosis

Is neonatal uterine bleeding responsible for early-onset endometriosis?

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