Preeclampsia (PE) is one of the most common pregnancy-related complications worldwide and currently lacks an effective treatment. While trophoblast cell dysfunction has been identified as the fundamental cause of PE, the underlying mechanisms remain unclear. Bone morphogenetic protein 5 (BMP5) is a secreted glycoprotein highly expressed in the placenta that is involved in cell proliferation, migration, and invasion. However, the role and mechanism of BMP5 glycosylation of trophoblast cell function remain unclear.

Cervical cancer is a leading cause of death in developing countries. Although the placenta is a tumor-like organ, the placental development, including invasive function, is well controlled. One mechanism is that extracellular vesicles (EVs) released from the placenta contribute to this regulation. Placental EVs carry functional proteins and regulatory RNAs. Our previous study reported that placental EVs inhibited ovarian cancer growth in vitro and in vivo.

Preeclamptic patients, both lean and obese, present with elevated leptin levels which are associated with the development of maternal endothelial dysfunction and adverse fetal outcomes, such as growth restriction, leading to low birth weight. Recent studies in pregnant mice demonstrate that mid-late gestation leptin infusion induces clinical characteristics of preeclampsia, including elevated maternal blood pressure, maternal endothelial dysfunction and fetal growth restriction. However, whether leptin triggers placental stress responses that contribute to adverse fetal outcomes as in preeclampsia is unknown.

Preeclampsia (PE) is a pregnancy-specific hypertensive disorder with inflammatory complications. There are no known placental histopathological features, which are unique to PE. It is often pooled with the fetal growth restriction (FGR) under a single umbrella pathophysiology, the maternal vascular malperfusion (MVM). The aim of this study is to assess the villous trophoblast and the villous tree quantitatively in PE placentas and to identify morpholgical correlates unique to PE.

Disturbed paternal epigenetic status of imprinted genes has been observed in infertility and recurrent spontaneous abortions. Shallow placentation has been associated with early-onset preeclampsia. Hence, the present study aimed to investigate the methylation patterns of imprinted genes involved in placental development, in the spermatozoa of partners of women experiencing preeclampsia.

Aspartame is a nonnutritive sweetener (NSS), which is widely used in foods and beverages worldwide. The safety of aspartame, a commonly used artificial sweetener, has been debated. Here, we investigated the potential effects and underlying mechanisms of aspartame consumption during pregnancy on placental dysfunction and birth outcomes.

Placenta-mediated diseases are associated with structural changes in the placenta. Quantitative Ultrasound (QUS) imaging measures the acoustic properties of the tissue, which are correlated to the underlying tissue structure. We aimed to develop and validate a diagnostic prediction model using QUS measurements for pre-eclampsia (PE) and small-for-gestational-age (SGA) fetuses/neonates.

To study if placental volume and placental to fetal ratio at gestational week (GW) 27 correlate with subsequent fetal growth. We also investigated whether the 1/3 smallest and 1/3 largest fetuses have different growth potential depending on placental volume.

Preeclampsia (PE) is a pregnancy complication marked by high blood pressure, posing risk to maternal and fetal health. "Genomic imprinting", an epigenetic phenomenon regulated by DNA methylation at Differently Methylated Regions (DMR's), influences placental development. Research on circulating extracellular vesicles (EVs) in PE suggests them as potential source for early biomarkers, but methylation status of EV-DNA in Preeclampsia is not reported yet.

Preeclampsia (PE) is a pregnancy-associated complication characterised by new-onset hypertension and proteinuria. This study explored the therapeutic potential of puerarin (Pue) in PE and investigated the underlying mechanism, with a focus on placental ferroptosis.

Gestational diabetes mellitus (GDM) is a common complication during pregnancy. The hyperglycemic stimulation of gestational diabetes inhibits the invasion of the placental trophoblast cells. Some studies have indicated that the senescence of trophoblast cells weakens their invasive capacity, while the mechanism of trophoblast cells senescence in GDM remain elusive.

A pilot study was carried out to test the efficacy of the autologous mitochondrial transfer therapy (AUGMENT) technique. No improvements in pregnancy rate, development, or embryo quality were observed in the AUGMENT-treated group versus the Control group in this study. The main objective of this research is to analyze whether AUGMENT technology did have any impact on the obstetric and perinatal outcomes of pregnancies and children resulting from treated oocytes.

Placental dysregulation frequently results in pregnancy complications that impact fetal well-being and potentially predispose the infant to diseases later in life. Thus, efforts to understand the molecular mechanisms underlying placental disorders are crucial to aid the development of effective treatments to restore placental function. Currently, the most common methods used for trophoblast-specific gene modulation in the laboratory are transgenic animals and lentiviral trophectoderm transduction. The generation of transgenic animal lines is costly and requires a considerable amount of time to generate and maintain, while the integration preference of lentiviruses, actively transcribed genes, may result in genotoxicity. Therefore, there is much interest in the development of non-viral in vivo transfection techniques for use in both research and clinical settings. Herein, we describe a non-viral, minimally invasive method for in vivo placental gene modulation through sonoporation, an ultrasound-mediated transfection technique wherein the application of ultrasound on target tissues is used to direct the uptake of DNA vectors. In this method, plasmids are bound to lipid microbubbles, which are then injected into the maternal bloodstream and ultimately delivered to the placenta when subjected to low-frequency ultrasound. Syncytiotrophoblasts are directly exposed to maternal blood and, therefore highly accessible to therapeutic agents in the maternal circulation. This technique can be used to modulate gene expression and, subsequently, the function of the placenta, circumventing the requirement to generate transgenic animals. Sonoporation also offers a safer alternative to existing viral techniques, making it not only an advantageous research tool but also a potentially adaptable technique in clinical settings.

Gestational diabetes mellitus (GDM) presents significant risks during pregnancy, including adverse perinatal outcomes and placental dysfunction. Impaired angiogenesis, involving crucial factors like Vascular Endothelial Growth Factor (VEGF), contributes to these complications. The Nrf2/Keap1 pathway, crucial for vascular redox homeostasis, has been linked to GDM-associated angiogenesis dysregulation.

The mechanisms leading to proper placentation are not fully understood. Extravillous trophoblasts (EVTs) are crucial for placentation through invasion and vascular remodeling, which, when impaired, promote a poor placentation. How autophagy could regulate EVTs function and the study of regulators of these processes, such as oxidized low-density lipoproteins (ox-LDL), could contribute to better understand events associated with pregnancy complications related to abnormal placental development, such as preeclampsia (PE).

Placenta accreta spectrum (PAS) disorders pose a grave threat to maternal life due to severe hemorrhage and the heightened risk of peripartum hysterectomy. Consequently, there's a pressing need for circulating biomarkers in clinical settings. MicroRNAs (miRNAs), being stable in peripheral circulation, hold promise as potential biomarkers for PAS.

Fetal and neonatal alloimmune thrombocytopenia (FNAIT) results from parental incompatibility in human platelet antigens (HPA) and subsequent maternal sensitization. The HPA-1a epitope is also expressed on placental tissue. Chronic placental inflammation and lower birth weight is observed more often in HPA-1a alloimmunized pregnancies, suggesting a placental component in the pathophysiology of FNAIT. Today, prediction of FNAIT severity is limited. The aim of the study was to investigate whether dysregulated maternal angiogenic proteins are associated with neonatal outcome in HPA-1a alloimmunized pregnancies.

The neonates' inflammatory response may in part be shaped during development by the placental epigenome, but evidence is scarce. We investigated the association between placental DNA methylation and pro-inflammatory proteins in cord blood.

The complex arborization of the feto-placental vasculature is crucial for optimal fetal nutrition, waste exchange and ultimately, development. Ethical and experimental limitations constrain research into the human placenta, hence experimental animal models such as mice and rats, are crucial to understand placental function. It is unclear how well the mouse and rat feto-placental vascular structure emulates human. Moreover, the implications of differences in vascular structure, especially in arborization, for placental function remain unclear.

An increasing amount of evidence suggests that immune responses may affect trophoblast functioning, which in turn may play a role in gestational disorders and fetal development. This systematic review offers the first summary of in vitro studies on the trophoblast response to immunological triggers, in conjunction with a risk of bias analysis. A search in Pubmed and Embase yielded 110 relevant studies. Primary trophoblasts were the most commonly used cell type, but trophoblast subtypes were not always defined. Similarly, the exact natures of trophoblast cell lines were sometimes unclear. Cytokines and Toll-like receptor agonists were often used as interventions, but most studies focused on a select few substances such as tumor necrosis factor-α and lipopolysaccharide. In regard to the outcome parameters, some important trophoblast functions, such as hormone production and barrier formation were underrepresented. Whether or not risk of bias was high varied strongly between types of bias. Risk of selection bias, for example, was usually low. However, none of the included studies mentioned blinding or plate randomization. Only a select few studies mentioned passage numbers, use of vehicle control or conflict of interest. In conclusion, better characterization of trophoblast subtypes and a broader range of studied interventions and outcome parameters would contribute to a more complete understanding of trophoblast responses to immune stimuli. Additionally, researchers are encouraged to replicate experiments and pay close attention when setting up and writing down methodologies, in order to improve the reproducibility and translatability of their work.