Role of Endometrial Autophagy in Physiological and Pathophysiological Processes

Yang, Shao-Liang; Wang, Haiyan; Li, Da‐Jin; Li, Ming‐Qing

doi:10.7150/jca.31742

Cited by 36 publications

(30 citation statements)

References 94 publications

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“…This process may be reversible, for example with progestin therapy acting as a suppressor, but mutations may occur under certain conditions within phenotypically normal endometrial glands. Over time, with the accumulation of subsequent genetic damage, not yet fully understood mutant clone of cells proliferates, which leads to histological changes and clinical mani- festations (abnormal uterine bleeding, characteristic ultrasonographic changes) malignancy is possible [12].…”

Section: Research Resultsmentioning

confidence: 99%

“…Cytoarchitectonics of endometrium in adenomyosis, characterized by the presence of heterotopic endometrial inclusions in the uterine myometrium and with impaired histological structure of the myometrium, accompanied by smooth muscle hyperplasia and changes in local immunity [10,25]. Heterotopias in adenomyosis are derivatives of the basal rather than the functional layer of the endometrium and, accordingly, respond worse to hormonal therapy than heterotopies of the external endometriosis [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

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Immunohistochemical features of benign endometrial hyperplasia in premenopausal women

Рожковська

Ломакіна

2020

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Hyperproliferative diseases of the endometrium play an important role in the structure of gynecological pathology, which are a spectrum of irregular morphological changes. Particularly difficult is evaluation of the phenotypic characteristics of the endometrium hyperplastic processes (EHP) in premenopausal women in the presence of an unstable menstrual cycle. Diagnosis and EHP prognosis remains a difficult task given that it can occur as focal or diffuse lesions with various structural and cytological differences.Objective of the study: to evaluate the immunohistochemical features (phenotypic variants) of benign endometrial hyperplasia in premenopausal women.Material and methods. 33 premenopausal women with abnormal uterine bleeding and verified benign endometrial hyperplasia were examined. Expression of the α-receptors for estrogens type 1 (ER1), progesterone receptors and Ki-67 nuclear protein in the endometrium stroma and glands was analyzed. Micromorphometry was performed and the D-score was calculated.Results. Prevalence of comorbid lesions in patients was the combination of endometrial hyperplasia and fibroids (51.4%), cases of abnormal uterine bleedings against submucosal fibroids (13.5%), endometrial polyps (8.1%), combinations of EHP and peritoneal endometriosis (10.8%), adenomyosis and myoma (8.1%), or other combinations of endometrial and myometrial proliferative pathology. D-score for surgery averaged 1.78 ± 0.11 indicating a low risk of malignancy. There were changes after treatment in the quantitative presentation of the studied proteins in stroma and endometrial glands. Thus, before treatment in the glands was determined up to 100% of cells containing ER1 in large quantities, while after treatment their number decreased by an average of 20%. Similar dynamics was observed with progesterone receptors activity.Conclusions. The main prognostic significant phenotypes of endometrial proliferative pathology have been identified. After removing of pathologically chanced endometrium and subsequent treatment with dydrogesterone during 6 months there is prognostically positive decreasing in the ER1 density as well as the Ki-67 protein expression

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Section: Research Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Immunohistochemical features of benign endometrial hyperplasia in premenopausal women

Рожковська

Ломакіна

2020

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“…In humans, where no such models are available, uterine and placental tissues obtained during various procedures have been used as the primary source for autophagy research. Review articles summarizing the potential role of endometrial or placental autophagy are recommended for further reading [ 33 , 34 ].…”

Section: Discussionmentioning

confidence: 99%

Autophagy in the uterine vessel microenvironment: Balancing vasoactive factors

Lim

2020

Clin Exp Reprod Med

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Autophagy, which has the literal meaning of self-eating, is a cellular catabolic process executed by arrays of conserved proteins in eukaryotes. Autophagy is dynamically ongoing at a basal level, presumably in all cells, and often carries out distinct functions depending on the cell type. Therefore, although a set of common genes and proteins is involved in this process, the outcome of autophagic activation or deficit requires scrutiny regarding how it affects cells in a specific pathophysiological context. The uterus is a complex organ that carries out multiple tasks under the influence of cyclic changes of ovarian steroid hormones. Several major populations of cells are present in the uterus, and the interactions among them drive complex physiological tasks. Mouse models with autophagic deficits in the uterus are very limited, but provide an initial glimpse at how autophagy plays a distinct role in different uterine tissues. Herein, we review recent research findings on the role of autophagy in the uterine mesenchyme in mouse models.

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“…Autophagy is beneficial to the process of endometrial decidualization. Impaired autophagy function of endometrial cells may cause infertility-related diseases such as endometriosis and polycystic ovary syndrome [32][33][34]. In order to verify the difference in trophoblasts autophagy levels is the cause of RSA production.…”

Section: Discussionmentioning

confidence: 99%

Autophagy suppression of trophoblast cells induces pregnancy loss by activating decidual NK cytotoxicity and inhibiting trophoblast invasion

Tan¹

Yang1

Wang

et al. 2019

Preprint

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Background: The crosstalk between trophoblast cells and decidual NK cells plays an important role in the establishment and maintenance of normal pregnancy. Recent studies have reported autophagy can induce immune tolerance at the maternal fetal interface, but the mechanism is largely unclear. Methods: Autophagy levels in the villi of normal and recurrent spontaneous abortion (RSA) patients were detected by transmission electron microscopy. In vivo and in vitro, the expression of killer molecules in NK cells was analyzed by flow cytometry (FCM). And the invasiveness of trophoblasts was tested by Cell invasion assay. Results: Compared with normal abortion patients, the level of autophagy in the villi of RSA patients was significantly decreased. In vitro experiments indicated that co-culture with autophagy suppression of trophoblasts (3-MA-pretreated trophoblasts) increased cytotoxicity of NK cell, which was mediated by the upregulation of insulin-like growth factor-2 (IGF-2). Meanwhile, autophagy suppression of trophoblasts led to a low level of Paternally Expressed Gene 10 (PEG10), leading to impaired cell invasion. In addition, NK cells educated by autophagy-inhibited trophoblasts further decreased the proliferation and invasiveness of trophoblasts. Injection with 3-MA in vivo , the cytotoxicity of uterine NK cells in pregnant mice and the embryo absorption rate were significantly increased. Conclusion: Autophagy suppression of trophoblasts should increase the cytotoxicity of NK cells and damage the trophoblasts invasion possibly by targeting IGF-2 and PEG10, respectively, which ultimately leads to miscarriage.

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Role of Endometrial Autophagy in Physiological and Pathophysiological Processes

Cited by 36 publications

References 94 publications

Immunohistochemical features of benign endometrial hyperplasia in premenopausal women

Immunohistochemical features of benign endometrial hyperplasia in premenopausal women

Autophagy in the uterine vessel microenvironment: Balancing vasoactive factors

Autophagy suppression of trophoblast cells induces pregnancy loss by activating decidual NK cytotoxicity and inhibiting trophoblast invasion

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