Endometrial receptivity in the eutopic endometrium of women with endometriosis: it is affected, and let me show you why

Lessey, Bruce A.; Kim, Julie

doi:10.1016/j.fertnstert.2017.05.031

Cited by 208 publications

(175 citation statements)

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“…Progesterone is essential for the establishment of pregnancy, so reduction in progesterone action would logically be associated with multiple down-stream changes in gene expression in the endometrium. In addition, inflammation is associated with P-resistance and an immune-regulated impact on the endometrium (39,40). BCL6 pairs with the histone deacetylase SIRT1, is centrally associated with epigenetic alterations in endometrial gene expression associated with endometriosis and likely has multiple effects on other key down-stream progesterone-regulated genes (18).…”

Section: Discussionmentioning

confidence: 99%

Endometrial BCL6 testing for the prediction of in vitro fertilization outcomes: a cohort study

Almquist

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Stone

et al. 2017

Fertility and Sterility

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Objective To evaluate endometrial BCL6 expression as a prognostic biomarker for In Vitro Fertilization (IVF) outcome in women with unexplained infertility (UI) prior to embryo transfer. Design Prospective cohort study. Setting University associated infertility clinic. Patients Women with UI for greater than 1 year. Interventions We studied women with UI who underwent testing for endometrial BCL6, in an LH-timed mid-luteal phase biopsy and completed an IVF cycle and embryo transfer. Main Outcome Measure(s) Clinical pregnancy rate (CPR) and live birth rate (LBR) per transfer was compared for women positive or negative for BCL6 expression. An abnormal BCL6 result was defined by an HSCORE (> 1.4). Results Women with normal and abnormal BCL6 and those who conceived or not had similar characteristics. Women with low levels of BCL6 expression had a significantly higher CPR (11/17; 64.7%; 95%CI: 41.3 to 82.6), compared to women with abnormal (high) BCL6 expression (9/52; 17.3%; 95%CI: 9.3 to 30.8). These results yield a relative risk (RR) of 0.267 (95%CI: 0.13 to 0.53; p = 0.0004) for those with normal BCL6 expression, an absolute benefit (AB) of 47.4% (95%CI: 22.5 to 72). LBR was also significantly higher in women with low BCL6 expression(10/17; 58.8; 95%CI: 36 to 78.4), compared to women with abnormal BCL6 expression (6/52; 11.5%; 95%CI: 5.4 to 23). The RR was 0.19 (95%CI: 0.08 to 0.45; p = 0.0002), yielding an AB of 47.3% (95%CI: 21.8 to 67.8). Conclusions Aberrant BCL6 expression (> 1.4 HSCORE) was strongly associated with poor reproductive outcomes in IVF cycles in women with UI.

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Section: Discussionmentioning

confidence: 99%

Endometrial BCL6 testing for the prediction of in vitro fertilization outcomes: a cohort study

Almquist

Likes

Stone

et al. 2017

Fertility and Sterility

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“…At the uterine level, inflammation induces an impairment of endometrial decidualization as a response to progesterone resistance due to the alteration in the function of PR. Therefore, the expression of progesterone-responsive genes is dysregulated during the implantation window, which comprises a period of 8-10 days after the luteinizing hormone (LH) surge (midsecretory phase) (11). Some of these altered genes encode biomarkers of endometrial receptivity (138), which are involved in embryo attachment and stimulation of decidua invasion, such as adhesion molecules (CAM family), cytokines, growth factors, and prostaglandins (11).…”

Section: Association Of Inflammation With Infertility In Patients Witmentioning

confidence: 99%

“…Especially in cases of deep endometriosis, the pain is due to an invasion of endometrial cells and pro-inflammatory mediators on the nerve fibers, which trigger a disorder of nociceptive modulation of pain increasing the intensity of the neuronal signal toward the somatosensory cerebral cortex (10). Infertility is another consequence of endometriosis, by reducing implantation capacity, increasing risk of pregnancy loss and physical obstruction imposed by endometriotic lesions (11). Moreover, endometriosis symptoms negatively influence women's life quality by affecting their productivity, social life, and emotional health (12).…”

Section: Introductionmentioning

confidence: 99%

Regulation of Inflammation Pathways and Inflammasome by Sex Steroid Hormones in Endometriosis

et al. 2020

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Endometriosis is a gynecological disorder characterized by the growth of endometrial tissue (glands and stroma) outside the uterus, mainly in the peritoneal cavity, ovaries, and intestines. This condition shows estrogen dependency and progesterone resistance, and it has been associated with chronic inflammation, severe pain, and infertility, which negatively affect the quality of life in reproductive women. The molecular mechanisms involved in the pathogenesis of endometriosis are not completely understood; however, inflammation plays a key role in the pathophysiology of the disease, mainly by altering the function of immune cells (macrophages, natural killer, and T cells) and increasing levels of pro-inflammatory mediators in the peritoneal cavity, endometrium, and blood. These immune alterations inhibit apoptotic pathways and promote adhesion and proliferation of endometriotic cells, as well as angiogenesis and neurogenesis in endometriotic lesions. It has been demonstrated that hormonal alterations in endometriosis are related to the inflammatory unbalance in this disease. Particularly, steroid hormones (mainly estradiol) promote the expression and release of pro-inflammatory factors. Excessive inflammation in endometriosis contributes to changes of hormonal regulation by modulating sex steroid receptors expression and increasing aromatase activity. In addition, dysregulation of the inflammasome pathway, mediated by an alteration of cellular responses to steroid hormones, participates in disease progression through preventing cell death, promoting adhesion, invasion, and cell proliferation. Furthermore, inflammation is involved in endometriosis-associated infertility, which alters endometrium receptivity by impairing biochemical responses and decidualization. The purpose of this review is to present current research about the role of inflammasome in the pathogenesis of endometriosis as well as the molecular role of sex hormones in the inflammatory responses in endometriosis.

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“…The endometrium is comprised of stromal cells and epithelial compartments. Notably, epithelial cells normally undergo anoikis, a mechanism of programmed cell death, upon detachment from the extracellular matrix [3]. Accordingly, the survival and migration of endometrial stromal cells (ESCs) outside the uterine cavity is the major cause for the development of endometriosis.…”

Section: Introductionmentioning

confidence: 99%

Effect of Mst1 on Endometriosis Apoptosis and Migration: Role of Drp1-Related Mitochondrial Fission and Parkin-Required Mitophagy

Zhao

Yang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Mitochondrial homeostasis is implicated in the development and progression of endometriosis through poorly defined mechanisms. Mst1 is the major growth suppressor related to cancer migration, apoptosis and proliferation. However, whether Mst1 is involved in endometriosis apoptosis and migration via regulating the mitochondrial function remains to be elucidated. Methods: Expression of Mst1 in endometriosis was examined via western blots. Cellular apoptosis was detected via MTT and TUNEL assay. Gain of function assay about Mst1 was conducted via adenovirus over-expression. Mitochondrial functions were evaluated via mitochondrial membrane potential JC-1 staining, ROS flow cytometry analysis, mPTP opening assessment and immunofluorescence of HtrA2/Omi. The mitophagy activity were examined via western blots and immunofluorescence. Results: First, we found that Mst1 was significantly downregulated in the ectopic endometrium of endometriosis compared to the normal endometrium. However, the recovery of Mst1 function was closely associated with the inability of endometrial stromal cells (ESCs) to migrate and survive. A functional study indicated that regaining Mst1 enhanced Drp1 post-transcriptional phosphorylation at Ser616 and repressed Parkin transcription activity via p53, leading to mitochondrial fission activation and mitophagy inhibition. Excessive Drp1-related fission forced the mitochondria to liberate HtrA2/Omi into the cytoplasm. Moreover, Mst1-induced defective mitophagy evoked cellular

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Endometrial receptivity in the eutopic endometrium of women with endometriosis: it is affected, and let me show you why

Cited by 208 publications

References 159 publications

Endometrial BCL6 testing for the prediction of in vitro fertilization outcomes: a cohort study

Endometrial BCL6 testing for the prediction of in vitro fertilization outcomes: a cohort study

Regulation of Inflammation Pathways and Inflammasome by Sex Steroid Hormones in Endometriosis

Effect of Mst1 on Endometriosis Apoptosis and Migration: Role of Drp1-Related Mitochondrial Fission and Parkin-Required Mitophagy

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