Maternal Uterus Research Articles

Nursing interventions in patients with incomplete abortion

Introduction: Incomplete abortion is defined as the presence of placental remains or fetal residues inside the maternal uterus before 22 weeks of gestation, which manifests with pain and vaginal bleeding apart from severe complications such as hemorrhage if a surgical procedure is not performed. immediate. Objective: To expose Nursing interventions in patients with incomplete abortion. Methodology: Qualitative study type unique clinical case, which is based on the Nursing Care Process method, included a 37-year-old female patient, applied the evaluation guide by functional patterns of Marjory Gordon, NANDA taxonomy, NOC, NIC and the evaluation of results according to the difference between the final and baseline scores. Results: Nine affected patterns were found, of which six patterns were prioritized, which were: Perceived health management, Nutritional-Metabolic, Activity-Exercise, Cognitive-Perceptive, Self-perception-Self-concept and Sexuality-Reproduction. Six nursing diagnoses were identified, the main diagnosis was considered: Acute pain and risk of complication: Hemorrhage, following the Area Model. A change score of +2 and +3 was obtained, which improved after the application of care. Conclusions: Clinical manifestations and possible complications of the patient with Incomplete abortion were identified, which were pain and hemorrhage, nursing care was essential and the evolution and prognosis of the patient largely depended on them. Therefore, it is necessary to strengthen the skills and expertise of the professional specialist in Obstetrics and Gynecology, all to provide quality care such as executing a rapid individualized response to improve the patient's health.

Shedding of Syncytiotrophoblast-Derived Extracellular Vesicles Is Increased in Placenta Previa and Accreta Spectrum

Placenta accreta spectrum (PAS) refers to excessive placental invasion into the maternal uterus and it is associated with high risk of obstetric haemorrhage and adverse maternal-neonatal outcomes. Currently, no specific circulating biomarkers of PAS have been identified. Given that in PAS disorders, the depth and the extension of placental invasion into the uterus are expected to be increased, in this study, we analysed plasma levels of syncytiotrophoblast-derived extracellular vesicles (STBEVs) in women with placenta previa (PP), at a high risk of PAS disorders, and pregnant women with normal placentation. Venous blood samples were collected from 35 women with ultrasonographic diagnosis of PP and 35 women with normal placentation, matched for gestational age. Plasma samples were ultracentrifuged at 120.000 g to collect extracellular vesicles (EVs). To identify and quantify plasma placenta–derived EVs (or STBEVs), EVs were analysed by flow cytometry using a monoclonal antibody against placental alkaline phosphatase (PLAP). Plasma levels of STBEVs were significantly higher in PP patients compared to controls. Plasma levels of STBEVs in women with PP and PAS showed a trend to a higher concentration compared to women with PP without PAS, although not reaching a statistical significance. Circulating STBEVs are potential candidates as biological markers to be integrated to ultrasonography in the antenatal screening programme for PAS. More studies are needed to confirm our observation in a larger cohort of patients and to analyse a possible association between high circulating levels of STBEVs and PAS.

Ultrasound manifestations and clinical analysis of 50 cases of heterotopic pregnancy.

To investigate the value of ultrasonography in the diagnosis of heterotopic pregnancy and the follow-up. A retrospective analysis of 50 cases of clinically diagnosed heterotopic pregnancy in our hospital was performed, the clinical characteristics and ultrasonographic manifestations of the patients were summarized, the reasons for initial ultrasound missed diagnosis and misdiagnosis were analyzed, and the pregnancy outcomes were followed up. Among the 50 cases, the initial ultrasound diagnoses of intrauterine pregnancy were all gestational sac type, 32 cases of ectopic pregnancy were located in the fallopian tube, and 10 cases were located in the uterine horn, 1 case at cervix, and 1 case at caesarean section scar. Forty-one cases were consistent with surgery and/or pathology, representing initial ultrasound diagnosis coincidence rate of about 82%. Six cases were missed in the initial ultrasound examination (12%), and three cases were misdiagnosed (6%). The maximum diameter of the intrauterine gestational sac was 9-48 mm, the average was about 24.90 ± 9.56 mm, the maximum diameter of the ectopic pregnancy gestational sac or mass was 11-63 mm, and the average was about 31.45 ± 13.82 mm (p < 0.05). Intrauterine pregnancy outcomes were followed up, 45 patients with complete data and 5 patients were lost to follow-up. The follow-up rate was about 90%. Combining the patient's medical history and clinical characteristics can reduce missed diagnosis and misdiagnosis of heterotopic pregnancy. Ultrasonography has important value in the assessment of intrauterine pregnancy growth and development, and the integrity of maternal uterus.

Characterization of fetal microchimeric immune cells in mouse maternal hearts during physiologic and pathologic pregnancies.

Introduction: During pregnancy, fetal cells can be incorporated into maternal tissues (fetal microchimerism), where they can persist postpartum. Whether these fetal cells are beneficial or detrimental to maternal health is unknown. This study aimed to characterize fetal microchimeric immune cells in the maternal heart during pregnancy and postpartum, and to identify differences in these fetal microchimeric subpopulations between normal and pregnancies complicated by spontaneous preterm induced by ascending infection. Methods: A Cre reporter mouse model, which when mated with wild-type C57BL/6J females resulted in cells and tissues of progeny expressing red fluorescent protein tandem dimer Tomato (mT+), was used to detect fetal microchimeric cells. On embryonic day (E)15, 104 colony-forming units (CFU) E. coli was administered intravaginally to mimic ascending infection, with delivery on or before E18.5 considered as preterm delivery. A subset of pregnant mice was sacrificed at E16 and postpartum day 28 to harvest maternal hearts. Heart tissues were processed for immunofluorescence microscopy and high-dimensional mass cytometry by time-of-flight (CyTOF) using an antibody panel of immune cell markers. Changes in cardiac physiologic parameters were measured up to 60days postpartum via two-dimensional echocardiography. Results: Intravaginal E. coli administration resulted in preterm delivery of live pups in 70% of the cases. mT + expressing cells were detected in maternal uterus and heart, implying that fetal cells can migrate to different maternal compartments. During ascending infection, more fetal antigen-presenting cells (APCs) and less fetal hematopoietic stem cells (HSCs) and fetal double-positive (DP) thymocytes were observed in maternal hearts at E16 compared to normal pregnancy. These HSCs were cleared while DP thymocytes persisted 28days postpartum following an ascending infection. No significant changes in cardiac physiologic parameters were observed postpartum except a trend in lowering the ejection fraction rate in preterm delivered mothers. Conclusion: Both normal pregnancy and ascending infection revealed distinct compositions of fetal microchimeric immune cells within the maternal heart, which could potentially influence the maternal cardiac microenvironment via (1) modulation of cardiac reverse modeling processes by fetal stem cells, and (2) differential responses to recognition of fetal APCs by maternal T cells.

Cow and management factors and their association with estimates of uterine size and position at the time of insemination of dairy cattle.

This study examines factors affecting uterine size and position determined at 30-36 days postpartum in dairy cattle. The final study population consisted of 328 dairy cows, all calving during the warm season. Uterus position (pelvic, pelvic-abdominal, abdominal) and uterus size (small, medium, large) was measured by ultrasound on Day 30-36 postpartum. Multiparous cows had a larger uterus positioned in the abdominal cavity (p = .03) and a male newborn was associated with a larger uterus (p = .022). The number of cows with the uterus in the abdominal cavity was higher among multiparous and high producer (p < .0001) cows. High producers were 0.41 times more likely to have a small uterus in a pelvic position. The most important finding of this study was that the delivery of a male dairy, rather than beef, calf was related to the least optimal maternal uterus size and position.

Review: Overview of the transcriptomic landscape in bovine blastocysts and elongated conceptuses driving developmental competence.

In cattle, pregnancy loss due to early embryonic mortality is a major concern that significantly impacts reproductive efficiency. Given the economic importance of cattle in livestock productivity, much research has been carried out to comprehend the regulatory mechanisms underlying this early embryo loss. Thus, understanding the molecular principles behind the reciprocal communication between the maternal uterus and the developing conceptus is paramount. Measurement of mRNA expression through a variety of techniques is widely used to unravel the complex and dynamic interaction between these two players. Development of high-throughput technologies, such as microarrays and RNA sequencing, have allowed global quantification of the full range of expressed mRNA, or transcriptome, of a biological sample. Therefore, numerous investigators have applied one or the other method to study the bovine embryo transcriptome at different developmental checkpoints and under different conditions. The goal of this article was to review studies involving the use of high-throughput techniques to study the transcriptome of the bovine embryo from the blastocyst (∼day 7) to the elongating conceptus stage (∼days 13-16) in terms of developmental capacity and the impact of procedures for in vitro embryo production. Furthermore, the differentially expressed genes reported by each study and enriched pathways were compared to determine common terms. The studies described here highlight differences in the transcriptome (i) between blastocysts with divergent ability to sustain a pregnancy, (ii) between age-matched elongated conceptuses with divergent developmental fates, and (iii) between blastocysts and elongated conceptuses produced in vitro or in vivo. Comparison between these works, supported by other studies involving transcriptomic data integration presented at the end of this review, highlights the involvement of pathways related to energy metabolism in embryonic competence, which may be altered because of the procedures involved in the in vitro production of embryos.

Human umbilical cord mesenchymal stem cell-derived extracellular vesicles loaded with TFCP2 activate Wnt/β-catenin signaling to alleviate preeclampsia.

Failures in invasive extravillous trophoblasts (EVTs) migration into the maternal uterus have been noticed in preeclampsia (PE). Human umbilical cord mesenchymal stem cell (hUCMSC)-derived extracellular vesicles (EVs) have been highlighted for the role as a potential therapeutic method in PE. This study intends to investigate the mechanistic basis of hUCMSCs-derived EVs loaded with bioinformatically identified TFCP2 in the activities of EVTs of PE. Primary human EVTs were exposed to hypoxic/reoxygenation (H/R) to mimic the environment encountered in PE. The in vivo PE-like phenotypes were induced in mice by reduced uterine perfusion pressure (RUPP) surgery. CCK-8, Transwell and flow cytometry assays were performed to detect proliferation, migration, invasion and apoptosis of H/R-exposed EVTs. More importantly, EVs were extracted from hUCMSCs and transduced with ectopically expressed TFCP2, followed by co-culture with EVTs. TFCP2 was found to be down-regulated in the preeclamptic placental tissues and in H/R-exposed EVTs. hUCMSCs-EVs loaded with TFCP2 activated the Wnt/β-catenin pathway, thereby promoting the proliferative, migratory, and invasive potential of EVTs. Furthermore, overexpression of TFCP2 alleviated PE-like phenotypes in mice, which was associated with activated Wnt/β-catenin pathway. From our data we conclude that hUCMSCs-EVs overexpressing TFCP2 may be instrumental for the therapeutic targeting and clinical management of PE.

Journey of the mouse primitive endoderm: from specification to maturation.

The blastocyst is a conserved stage and distinct milestone in the development of the mammalian embryo. Blastocyst stage embryos comprise three cell lineages which arise through two sequential binary cell fate specification steps. In the first, extra-embryonic trophectoderm (TE) cells segregate from inner cell mass (ICM) cells. Subsequently, ICM cells acquire a pluripotent epiblast (Epi) or extra-embryonic primitive endoderm (PrE, also referred to as hypoblast) identity. In the mouse, nascent Epi and PrE cells emerge in a salt-and-pepper distribution in the early blastocyst and are subsequently sorted into adjacent tissue layers by the late blastocyst stage. Epi cells cluster at the interior of the ICM, while PrE cells are positioned on its surface interfacing the blastocyst cavity, where they display apicobasal polarity. As the embryo implants into the maternal uterus, cells at the periphery of the PrE epithelium, at the intersection with the TE, break away and migrate along the TE as they mature into parietal endoderm (ParE). PrE cells remaining in association with the Epi mature into visceral endoderm. In this review, we discuss our current understanding of the PrE from its specification to its maturation. This article is part of the theme issue 'Extraembryonic tissues: exploring concepts, definitions and functions across the animal kingdom'.

Nanotechnologies in Obstetrics and Cancer during Pregnancy: A Narrative Review.

Nanotechnology, the art of engineering structures on a molecular level, offers the opportunity to implement new strategies for the diagnosis and management of pregnancy-related disorders. This review aims to summarize the current state of nanotechnology in obstetrics and cancer in pregnancy, focusing on existing and potential applications, and provides insights on safety and future directions. A systematic and comprehensive literature assessment was performed, querying the following databases: PubMed/Medline, Scopus, and Endbase. The databases were searched from their inception to 22 March 2022. Five independent reviewers screened the items and extracted those which were more pertinent within the scope of this review. Although nanotechnology has been on the bench for many years, most of the studies in obstetrics are preclinical. Ongoing research spans from the development of diagnostic tools, including optimized strategies to selectively confine contrast agents in the maternal bloodstream and approaches to improve diagnostics tests to be used in obstetrics, to the synthesis of innovative delivery nanosystems for therapeutic interventions. Using nanotechnology to achieve spatial and temporal control over the delivery of therapeutic agents (e.g., commonly used drugs, more recently defined formulations, or gene therapy-based approaches) offers significant advantages, including the possibility to target specific cells/tissues of interest (e.g., the maternal bloodstream, uterus wall, or fetal compartment). This characteristic of nanotechnology-driven therapy reduces side effects and the amount of therapeutic agent used. However, nanotoxicology appears to be a significant obstacle to adopting these technologies in clinical therapeutic praxis. Further research is needed in order to improve these techniques, as they have tremendous potential to improve the accuracy of the tests applied in clinical praxis. This review showed the increasing interest in nanotechnology applications in obstetrics disorders and pregnancy-related pathologies to improve the diagnostic algorithms, monitor pregnancy-related diseases, and implement new treatment strategies.

The environments of reproductive and birth defects research in the U.S. and West Germany (c. 1955–1975)

Most historiographies of the crossroads of environmental and reproductive health in 20th century start and end with the case of thalidomide. Despite its global scope, thalidomide today stands for sharp contrasts: in the numbers of victims, in institutional responses to the disaster, and also—more generally—in regulatory approaches to potential risks and national cultures of reproductive justice and disability rights. This paper takes a closer look at two countries that have been seen as emblematic of this divide in regulatory frameworks, despite similarities and interconnections in other areas, such as (pharma)industrial production, science, and robust feminist environmental health movements: the U.S. and West Germany. It argues that thalidomide needs to be historically contextualized within a broad framework of concepts and models of environment from research on exogenous reproductive effects. To do so, it reconstructs what counted as environment in research on reproductive health and birth defects in these two national settings in the postwar decades. It looks at transformations made across multifaceted initiatives, studying collective landscapes and workplaces as potentially dangerous “outer worlds,” as well as smaller scale and more individualized environments, i.e., the maternal metabolism, uterus, lifestyle, or social interactions. The article thereby aims to explicate concepts and debates about the environment that influenced later national divisions in politics of science and technology, hinting of the democratic challenges these posed.

Efficient cell chatting between embryo and uterus ensures embryo implantation

Embryo implantation is one of the hottest topics during female reproduction since it is the first dialogue between maternal uterus and developing embryo whose disruption will contribute to adverse pregnancy outcome. Numerous achievements have been made to decipher the underlying mechanism of embryo implantation by genetic and molecular approaches accompanied with emerging technological advances. In recent decades, raising concepts incite insightful understanding on the mechanism of reciprocal communication between implantation competent embryos and receptive uterus. Enlightened by these gratifying evolvements, we aim to summarize and revisit current progress on the critical determinants of mutual communication between maternal uterus and embryonic signaling on the perspective of embryo implantation to alleviate infertility, enhance fetal health, and improve contraceptive design.

A Leukocyte Migration Assay Assists Understanding of Interleukin-1β-Induced Leukocyte Migration Into Preterm Mouse Uterus.

Neutrophils and other leukocytes invade the mouse uterus at term birth, which is normal for activating the uterus for labor. To better understand the regulation of this migration at term and interleukin (IL)-1β—induced preterm birth, we developed a mouse leukocyte migration assay (mLMA) and used it with rytvela, an IL-1 receptor allosteric antagonist. The mLMA uses term peripheral blood leukocytes that migrate in a Boyden chamber in response to a chemoattractant. We tested several mouse uterine tissues after homogenization and sedimentation of debris for chemoattractant activity. The most active chemoattractant homogenate came from the mouse lower uterus on gestational day (GD) 18.5. Using flow cytometry, we demonstrated that 99% of the cells that migrate are neutrophils. IL-1β administered on GD 16 stimulated neutrophil migration and invasion into the uterus and the fetal brain along with preterm birth on GD 17. Preterm birth and the increased leukocyte invasion of the maternal uterus and fetal brain were all blocked by the co-administration of rytvela. To test where the site of IL-1β action might be, we examined the potency of lower uterine chemoattractant and the activation of leukocytes following IL-1β +/- rytvela administration. IL-1β did not increase lower uterus homogenate chemoattractant activity, but it significantly (p < 0.05) increased leukocyte activation as defined by cytokine and chemokine expression. Rytvela blocked this activation of leukocytes by IL-1β. We conclude that IL-1β stimulates preterm birth in mice by increasing leukocyte activation leading to increased uterine and fetal brain leukocyte invasion.

Folic Acid Levels During Pregnancy Regulate Trophoblast Invasive Behavior and the Possible Development of Preeclampsia.

BackgroundOne of the unique features of placentation is its similarity to tumorigenesis yet being very well regulated. It allows rapid proliferation, migration, and invasion of mononuclear trophoblast cells into the maternal uterus and remodeling the maternal vasculature. This pseudomalignant nature of trophoblastic cells is strictly regulated and its importance becomes evident in abnormal pregnancies that are characterized by aberrant trophoblast proliferation/invasion like preeclampsia. In addition to this, the importance of folic acid supplementation during pregnancy is well documented. We aimed to analyze the molecular and epigenetic regulation of the pseudomalignant nature of placentation via folic acid levels.MethodsPlacental tissue samples were collected from different pregnancies in three different gestational stages. We estimated the impact of folic acid levels on global methylation, LINE1 methylation, and expression of DNMTs in all three gestational stages in pregnant women and preeclampsia pregnancies. We also analyzed the effect of folic acid supplementation on trophoblastic invasion using placental derived cells viz, JEG-3 and HTR-8/SVneo cell line and verified the molecular and epigenetic mechanisms involved in this regulation.ResultsDevelopment of preeclampsia was observed to be associated with lower folate levels in placental tissue, higher global methylation level, and higher expression of DNMT1and DNMT3A. Folic acid supplementation was found to increase the invasive potential of placental trophoblasts by almost two folds which were associated with the decreased expression of tumor suppressor genes and tissue inhibitors of matrix metalloproteinases; and increased expression of oncogenes, telomerase gene, and matrix metalloproteinases. These folic acid-mediated changes were observed to be regulated by CpG methylation in the case of many genes. Folic acid supplementation was also observed to significantly decrease global methylation in placental trophoblasts related to decreasing expression of DNMT1 and DNMT3A.ConclusionLower folic acid levels are associated with preeclampsia development and folic acid supplementation regulates the invasive potential of placental trophoblasts as mediated by various epigenetic changes in the placenta suggesting the protective effect of folic acid against preeclampsia.

A microphysiological model of human trophoblast invasion during implantation

Successful establishment of pregnancy requires adhesion of an embryo to the endometrium and subsequent invasion into the maternal tissue. Abnormalities in this critical process of implantation and placentation lead to many pregnancy complications. Here we present a microenigneered system to model a complex sequence of orchestrated multicellular events that plays an essential role in early pregnancy. Our implantation-on-a-chip is capable of reconstructing the three-dimensional structural organization of the maternal-fetal interface to model the invasion of specialized fetal extravillous trophoblasts into the maternal uterus. Using primary human cells isolated from clinical specimens, we demonstrate in vivo-like directional migration of extravillous trophoblasts towards a microengineered maternal vessel and their interactions with the endothelium necessary for vascular remodeling. Through parametric variation of the cellular microenvironment and proteomic analysis of microengineered tissues, we show the important role of decidualized stromal cells as a regulator of extravillous trophoblast migration. Furthermore, our study reveals previously unknown effects of pre-implantation maternal immune cells on extravillous trophoblast invasion. This work represents a significant advance in our ability to model early human pregnancy, and may enable the development of advanced in vitro platforms for basic and clinical research of human reproduction.

A History of Neonatal Uterine Bleeding and Its Significance

Bleeding in newborns and young girls fascinated writers for more than a millennium. Initially, there was confusion between neonatal bleeding, early menstruation due to precocious puberty, and hemorrhage due to disease. During the 19th century descriptions appeared of what is referred to today as ‘neonatal menstruation’ or ‘neonatal uterine bleeding’. By the turn of the century, Halban linked bleeding to active substances present during pregnancy and hypothesized that, while the maternal uterus reacts with decidua formation, the “weaker” fetal uterus reacts only with menstrual-like changes. Despite this clear description, several alternative theories endured for decades. Bleeding was believed to be due to a ‘catarrhal’ or neoplastic state of the genital tract, pulmonary circulatory disorder, congenital heart malformations, closure of the umbilical cord or affections of the intestine. During the 1950s, progesterone response and resistance were proposed to explain the pathogenesis of bleeding and its low incidence. The fetal endometrium is resistant to the high circulating progesterone. A decidual response is infrequent and results in menstrual shedding upon progesterone withdrawal after birth. Further research linked fetal stress consequent to pregnancy complications and post-maturity to increased incidence and preterm birth to reduced incidence of neonatal uterine bleeding.

From the maternal uterus to the "uterus device"? Ethical and scientific considerations on partial ectogenesis.

The article aims to elaborate the progress made in partial ectogenesis research on sheep as well as human embryos. Since the ban on embryos experimentation after the 14-day window is a major roadblock in terms of partial ectogenesis research, the authors have weighed the possibility that such a ban could be reconsidered. In favor of easing such a restriction, it may be argued that: (a) unlike the Catholic approach, prevalent ethics precepts hold that the embryo's interest ought to be balanced against the interests of the other parties involved; (b) an extension of the 14-day deadline would no longer make ethically untenable practices acceptable; hence, the "slippery slope" argument, although generally worthy, would not conclusively apply to partial ectogenesis; (c) in mainstream embryo research efforts, there is a conflict between the lives of embryos and the health of individuals already born; as for partial ectogenesis, however, such a conflict would be between the lives of embryos and the lives of fetuses which would not survive otherwise. Still, in light of the embryo's status as a human being, the authors conclude that such research practices should only be allowed on supernumerary embryos.

Extravillous trophoblast migration and invasion: Impact of environmental chemicals and pharmaceuticals

During pregnancy, the migration and invasion of extravillous trophoblasts (EVTs) into the maternal uterus is essential for proper development of the placenta and fetus. During the first trimester, EVTs engraft and remodel maternal spiral arteries allowing for efficient blood flow and the transfer of essential nutrients and oxygen to the fetus. Aberrant migration of EVTs leading to either shallow or deep invasion into the uterus has been implicated in a number of gestational pathologies including preeclampsia, fetal growth restriction, and placenta accreta spectrum. The migration and invasion of EVTs is well-coordinated to ensure proper placentation. However, recent data point to the ability of xenobiotics to disrupt EVT migration. These xenobiotics include heavy metals, endocrine disrupting chemicals, and organic contaminants and have often been associated with adverse pregnancy outcomes. In most instances, xenobiotics appear to reduce EVT migration; however, there are select examples of enhanced motility after chemical exposure. In this review, we provide an overview of the 1) current experimental approaches used to evaluate EVT migration and invasion in vitro, 2) ability of environmental chemicals and pharmaceuticals to enhance or retard EVT motility, and 3) signaling pathways responsible for altered EVT migration that are sensitive to disruption by xenobiotics.

Porcine uterine luminal fluid-derived extracellular vesicles improve conceptus-endometrial interaction during implantation

Successful implantation of porcine conceptus requires synergistic interaction with various signal molecules in the maternal uterus. Extracellular vesicles (EVs) in uterine luminal fluid (ULF) of mice play important roles in conceptus development. However, studies have not explored the roles of extracellular vesicles (EV) in ULF of pigs. The aim of this study was to identify characteristics, origin, and roles of ULF-derived EVs on day 9 of the estrous cycle and on day 9,12 and 15 of pregnancy in pigs. Western blot, BCA assay and HE staining analysis showed increase in EVs concentration in ULF began from day 12 of pregnancy. Immunofluorescence staining and transmission electron microscopy analysis showed that EVs were mainly derived from endometrial epithelial cells. Fluorescent labeling, CCK-8 and transwell migration assays showed that these EVs were delivered to the trophoblast or parthenogenetic activation embryos to regulate proliferation and migration of trophoblast cells. A total of 305 miRNAs were identified using small RNA sequencing analysis. Functional enrichment analysis showed that miRNAs in these EVs potentially play vital regulatory functions in EV transportation or conceptus implantation. QRT-PCR analysis was used to further verify the RNA-seq data. The findings of this study provide information on the functions of porcine ULF-derived EVs and provide a reference dataset for future translational studies on porcine ULF-derived EVs.

Interleukin-15 in Outcomes of Pregnancy.

Interleukin-15 (IL-15) is a pleiotropic cytokine that classically acts to support the development, maintenance, and function of killer lymphocytes. IL-15 is abundant in the uterus prior to and during pregnancy, but it is subject to tight spatial and temporal regulation. Both mouse models and human studies suggest that homeostasis of IL-15 is essential for healthy pregnancy. Dysregulation of IL-15 is associated with adverse outcomes of pregnancy. Herein, we review producers of IL-15 and responders to IL-15, including non-traditional responders in the maternal uterus and fetal placenta. We also review regulation of IL-15 at the maternal–fetal interface and propose mechanisms of action of IL-15 to facilitate additional study of this critical cytokine in the context of pregnancy.

Placental trophoblast cell-derived exosomal microRNA-1290 promotes the interaction between endometrium and embryo by targeting LHX6

Communication between the maternal uterus and the embryo is vital for a successful pregnancy. Exosomes, subtypes of extracellular vesicles comprising many bioactive factors, regulate the early stages of pregnancy, specifically during embryo implantation. Nevertheless, the mechanism by which exosomal microRNAs (miRNAs) derived from placental trophoblasts regulate embryo implantation remains elusive. We isolated and identified exosomes derived from placental trophoblast cells (HTR8/SVneo). Subsequently, we evaluated the loading miRNA in exosomes by small RNA sequencing. Consequently, we showed that trophoblast cell-derived exosomes could transfer to endometrial epithelial cells. Besides, these exosomes promoted the epithelial-mesenchymal transition (EMT) as well as migration of endometrial cells and were implicated in the regulation of inflammation. Further, the specific miRNAs were screened in exosomes, and as a result, miRNA (miR)-1290 was enriched specifically in exosomes. miR-1290 promoted the expression of inflammatory factors (interleukin [IL]-6 and IL-8) and migration of endometrial epithelial cells. In addition, exosomal miR-1290 promoted angiogenesis in vitro. More importantly, by targeting LHX6, trophoblast HTR8/SVneo cell-derived exosomal miR-1290 promoted the EMT process of endometrial epithelial cell HEC-1-A. Altogether, our findings provide novel insights into the mechanism of trophoblast cell-derived exosomes during embryo implantation.