miR-548az-5p induces amniotic epithelial cell senescence by regulating KATNAL1 expression in labor.

Amniotic fluid exosomes (AF-Exos) from term labor (TL) cause amniotic membrane senescence and induce labor. However, the intrinsic mechanism through which this occurs remains unknown. Therefore, we performed microRNA (miRNA) microarray chip screening of AF-Exos obtained from TL and terms not in labor and discovered that the expression of miR-548az-5p was significantly upregulated in TL.

Hsa-miR-3928-3p targets the CCL3/CCR5 axis to induce amniotic epithelial cell senescence involved in labor initiation.

Introduction: Senescence in human amniotic epithelial cells (hAECs) and increased sterile inflammation in the amniotic cavity can lead to the initiation of term labor (TL). We investigated the possible roles of hsa-miR-3928-3p and chemokine ligand 3 (CCL3) in labor initiation and the underlying molecular mechanisms.

Methods: Microarray chip screening was used to analyse the differential expression of miRNAs in amniotic fluid exosomes from women in TL and term not-in-labor.

The role of aryl hydrocarbon receptors in nutrient metabolism and immune regulation at the maternal-fetal interface.

The maternal-fetal interface is composed of the placenta, which is affiliated with the fetus, and the maternal decidua. During pregnancy, the placenta is mainly responsible for nutrient transport and immune tolerance maintenance, which plays a key role in fetal growth and development and pregnancy maintenance. The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that exists in various cell types at the maternal-fetal interface and is involved in multiple cellular processes.

Exosomal encapsulation of miR-3198 promotes proliferation and migration of trophoblasts in preeclampsia.

Purpose: Preeclampsia (PE) is a vascular remodeling disorder cloesly linked to trophoblast dysfunction, involving defects in their proliferation, migration, and apoptosis. Maternal exosomal microRNAs (miRNAs) have been reported to play pivotal roles in the development of PE. However, the mechanism underlying the role of maternal exosomes in trophoblast dysfunction regarding the development of PE is poorly understood.

Decidual macrophage: a reversible role in immunotolerance between mother and fetus during pregnancy.

The tolerance of the semi-allogeneic fetus by the maternal immune system is an eternal topic of reproductive immunology for ensuring a satisfactory outcome. The maternal-fetal interface serves as a direct portal for communication between the fetus and the mother. It is composed of placental villi trophoblast cells, decidual immune cells, and stromal cells.

Preeclampsia impedes foetal kidney development by delivering placenta-derived exosomes to glomerular endothelial cells.

Background: Foetal renal dysplasia is still the main cause of adult renal disease. Placenta-derived exosomes are an important communication tool, and they may play an important role in placental (both foetal and maternal) function. We hypothesize that in women with preeclampsia, foetal renal dysplasia is impeded by delivering placenta-derived exosomes to glomerular endothelial cells.

Exosomal miR-146a-5p derived from human umbilical cord mesenchymal stem cells can alleviate antiphospholipid antibody-induced trophoblast injury and placental dysfunction by regulating the TRAF6/NF-κB axis.

Exosomes originating from human umbilical cord mesenchymal stem cells (hucMSC-exos) have become a novel strategy for treating various diseases owing to their ability to regulate intercellular signal communication. However, the potential of hucMSC-exos to improve placental injury in obstetric antiphospholipid syndrome and its underlying mechanism remain unclear. Our objective was to explore the potential application of hucMSC-exos in the treatment of obstetric antiphospholipid syndrome and elucidate its underlying mechanism.

Unraveling the gut microbiota and short-chain fatty acids characteristics and associations in a cancer cachexia mouse model.

Objective: Cachexia is a common pathological condition in cancer patients, affecting prognosis and treatment outcomes. The relationship between cachexia and gut microbiota and short-chain fatty acids (SCFAs) remains understudied. This research aimed to establish a cachexia mouse model and explore the gut microbiota-SCFAs connection.

MiR-218-5p promotes trophoblast infiltration and inhibits endoplasmic reticulum/oxidative stress by reducing UBE3A-mediated degradation of SATB1.

This research evaluated the effects of miR-218-5p on trophoblast infiltration and endoplasmic reticulum/oxidative stress during preeclampsia (PE). The expression of miR-218-5p and special AT-rich sequence binding protein 1 (SATB1) in placental tissues from 25 patients with PE and 25 normal pregnant subjects was determined using qRT-PCR and western blotting. Cell invasion and cell migration were detected by performing Transwell assays and scratch assays, respectively.

Influence of placental exosomes from early onset preeclampsia women umbilical cord plasma on human umbilical vein endothelial cells.

Background: Early onset preeclampsia (EOSP, PE) is characterized by hypertension, proteinuria, and endothelial dysfunction. Oxidative stress-induced trophoblast dysfunction is a major pathology in PE. Placental exosomes are extracellular vesicles that are involved in "mother-placenta-foetal communication" and can regulate the biological functions of endothelial cells.

Single-cell transcriptomics dissects epithelial heterogeneity in HPV cervical adenocarcinoma.

The intra- and intertumoral heterogeneity of epithelial cells in human papillomavirus (HPV ) cervical adenocarcinoma (CEAD) remains largely unknown. To investigate this issue, we performed single-cell RNA sequencing on 19 229 epithelial cells sorted from three tumor samples of three patients with HPV CEAD. Six epithelial subclusters (Epi1-Epi6) were identified that showed distinct gene expression.

Fetal Lung-Derived Exosomes in Term Labor Amniotic Fluid Induce Amniotic Membrane Senescence.

The mechanism of parturition is still unclear. Evidence has shown that delivery is associated with cellular senescence of the amniotic membrane. We isolated fetal lung-associated exosomes from the amniotic fluid from term labor (TL-exos) and verified that the exosomes can cause primary human amniotic epithelial cell (hAEC) senescence and apoptosis and can release higher levels of senescence-associated secretory phenotype (SASP)-related molecules and proinflammatory damage-associated molecular patterns (DAMPs) than exosomes isolated from the amniotic fluid from term not in labor (TNIL-exos).

Distinguishing placenta accreta from placenta previa via maternal plasma levels of sFlt-1 and PLGF and the sFlt-1/PLGF ratio.

Introduction: Our study aimed to distinguish patients with placenta accreta (crete, increta, and percreta) from those with placenta previa using maternal plasma levels of soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PLGF) and the sFlt-1/PLGF ratio.

Methods: We obtained maternal plasma from 185 women in late pregnancy and sorted them into three groups: 72 women with normal placental imaging results (control group), 50 women with placenta previa alone (PP group), and 63 women with placenta previa and placenta accreta (PAS group). The concentrations of sFlt-1 and PLGF in the maternal plasma were measured using ELISA kits and the sFlt-1/PLGF ratio was calculated.