Hyperlipidemia negatively impacts implantation by dysregulating tight junction and Claudin-3 and Claudin-4 expression in the endometrium.

被引量：- 发表：1970

Linking reproductive tract microbiota to premature ovarian insufficiency: Pathophysiological mechanisms and therapies.

Over the past decade, research on the human microbiota has become a hot topic. Among them, the female reproductive tract (FRT) also has a specific microbiota that maintains the body's health and dynamic balance, especially in the reproductive aspect. When the FRT ecosystem is dysregulated, changes in immune and metabolic signals can lead to pathological and physiological changes such as chronic inflammation, epithelial barrier disruption, changes in cell proliferation and apoptosis, and dysregulation of angiogenesis and metabolism, thereby causing disruption of the female endocrine system. Premature ovarian insufficiency (POI), a clinical syndrome of ovarian dysfunction, is primarily influenced by immune, genetic, and environmental factors. New evidence suggests that dysbiosis of the FRT microbiota and/or the presence of specific bacteria may contribute to the occurrence and progression of POI. This influence occurs through both direct and indirect mechanisms, including the regulation of estrogen metabolism. The use of probiotics or microbiota transplantation to regulate the microbiome has also been proven to be beneficial in improving ovarian function and the quality of life in women with premature aging. This article provides an overview of the interrelationships and roles between the FRT microbiome and POI in recent years, to fully understand the risk factors affecting female reproductive health, and to offer insights for the future diagnosis, treatment, and application of the FRT microbiome in POI patients.

被引量：- 发表：1970

Angiotensin II type-1 receptor autoantibody positively correlates with the rate of metaphase I oocytes in infertility with ovulatory disorder.

The renin-angiotensin system (RAS) plays an important role in reproductive function. Our previous study identified that angiotensin II type-1 receptor autoantibody (AT1-AA), an autoantibody that activates RAS, was closely associated with infertility. However, its distribution in different types of infertility remained unclear. This study was designed to explore the distribution of AT1-AA in infertile patients and the connections between AT1-AA and oocyte development and pregnancy outcome. A total of 184 infertile women participated, with samples collected from peripheral venous blood. ELISA was used to detect AT1-AA levels in their sera. It was observed that the proportion of ovulation-disorder factors in AT1-AA-positive group was significantly higher than that in negative group (P=0.001). In 59 infertile women with ovulatory disorders, compared with negative group, AT1-AA-positive group had lower rate of retrieval (P=0.032) and metaphase II (MII) oocytes (P=0.011) but higher proportion of metaphase I (MI) oocytes (P=0.019). A negative correlation was found between the levels of AT1-AA and rate of retrieval and MII oocytes (P=0.027; P=0.043), whereas a positive correlation was observed with the proportion of MI oocytes (P=0.002). Moreover, a specific predictive value for proportion of reaching MII and MI oocytes was exhibited by AT1-AA (P < 0.01; P < 0.05). But no significant difference in embryonic parameters or pregnancy outcomes between two groups was observed (P > 0.05). This study revealed that serum AT1-AA levels were significantly increased in infertile women with ovulatory disorders and positively correlated with proportion of MI oocytes, but not associated with outcomes of assisted reproduction.

被引量：- 发表：1970

Glutamine metabolism promotes human trophoblast cell invasion via COL1A1 mediated by PI3K-AKT pathway.

Abnormal trophoblast invasion function is an important cause of recurrent spontaneous abortion (RSA). Recent research has revealed a connection between glutamine metabolism and RSA. However, the interplay between these three factors and their related mechanisms remains unclear. To address this issue, we collected villus tissues from 10 healthy women with induced abortion and from 10 women with RSA to detect glutamine metabolism. Then, the trophoblast cell line HTR-8/SVneo was used in vitro to explore the effect of glutamine metabolism on trophoblast cells invasion, which was tested by transwell assay. We found that the concentration of glutamine in the villi of the normal pregnancy group was significantly higher than that in the RSA group. Correspondingly, the expression levels of key enzymes involved in glutamine synthesis and catabolism, including glutamine synthetase and glutaminase, were significantly higher in the villi of the normal pregnancy group. Regarding trophoblast cells, glutamine markedly enhanced the proliferative and invasive abilities of HTR-8/SVneo cells. Additionally, collagen type I alpha 1 (COL1A1) was confirmed to be a downstream target of glutamine, and glutamine also activated the PI3K-AKT pathway in HTR-8/SVneo cells. These findings indicate that glutamine metabolism facilitates the invasion of trophoblasts by up-regulating COL1A1 expression through the activation of the PI3K-AKT pathway, but the specific mechanism of COL1A1 requires further study.

被引量：- 发表：1970

Progesterone and estradiol alleviate Poly I:C-induced immune response in endometrial stromal cells.

Progesterone (P) and estradiol (E2) regulate the immune status of the uterus. However, whether P and E2 can affect the immune response of endometrial cell is still unknown. In the study, primary endometrial stromal cells (EndSCs) were treated with Poly(I:C), the pathogen-associated molecular pattern of double-stranded RNA (dsRNA) virus, to induce immune response, and then EndSCs were stimulated with P or/and E2. The results showed Poly(I:C) up-regulated the expression of immune cytokines IL-6, IL-8, IL-1β and TNF-α, and significantly down-regulated the expression of ERα and PGRMC1 in EndSCs. Moreover, P or low-dose of E2 attenuate Poly(I:C)-induced immune response, and then the synergistic effects of P and E2 decreased expression of ERα, ERβ and PGR, and alleviate the decease of PGRMC1 induced by Poly(I:C), but not alleviate the decease of ERα caused by Poly(I:C). The result provides a steroid therapeutic method to suppress dsRNA virtues-induced immune response through the synergistic effect of P and E2 on endometrial stromal cells.

被引量：- 发表：1970