IL-1β Induces Human Endothelial Surface Expression of IL-15 by Relieving let-7c-3p Suppression of Protein Translation.

Expression of IL-15 on the surface of human graft endothelial cells (ECs) bound to the IL-15Rα subunit can increase the activation of CTLs, potentiating allograft rejection. Our previous work showed that surface expression of this protein complex could be induced by alloantibody-mediated complement activation through increased IL-1β synthesis, secretion, and autocrine/paracrine IL-1-mediated activation of NF-κB. In this article, we report that cultured human ECs express eight differently spliced IL-15 transcripts.

Complement Membrane Attack Complexes Disrupt Proteostasis to Function as Intracellular Alarmins.

Internalized pools of membrane attack complexes (MACs) promote NF-kB and dysregulated tissue inflammation. Here, we show that C9, a MAC-associated protein, promotes loss of proteostasis to become intrinsically immunogenic. Surface-bound C9 is internalized into Rab5 + endosomes whose intraluminal acidification promotes C9 aggregates.

A ZFYVE21-Rubicon-RNF34 signaling complex promotes endosome-associated inflammasome activity in endothelial cells.

Internalization of complement membrane attack complexes (MACs) assembles NLRP3 inflammasomes in endothelial cells (EC) and promotes IL-β-mediated tissue inflammation. Informed by proteomics analyses of FACS-sorted inflammasomes, we identify a protein complex modulating inflammasome activity on endosomes. ZFVYE21, a Rab5 effector, partners with Rubicon and RNF34, forming a "ZRR" complex that is stabilized in a Rab5- and ZFYVE21-dependent manner on early endosomes.

Hedgehog-induced ZFYVE21 promotes chronic vascular inflammation by activating NLRP3 inflammasomes in T cells.

The zinc finger protein ZFYVE21 is involved in immune signaling. Using humanized mouse models, primary human cells, and patient samples, we identified a T cell-autonomous role for ZFYVE21 in promoting chronic vascular inflammation associated with allograft vasculopathy. Ischemia-reperfusion injury (IRI) stimulated endothelial cells to produce Hedgehog (Hh) ligands, which in turn induced the production of ZFYVE21 in a population of T memory cells with high amounts of the Hh receptor PTCH1 (PTCH cells, CD3CD4CD45ROPTCH1PD-1), vigorous recruitment to injured endothelia, and increased effector responses in vivo.

WTAP dysregulation-mediated HMGN3-m6A modification inhibited trophoblast invasion in early-onset preeclampsia.

Early-onset preeclampsia (ePE) originates from abnormal implantation and placentation that involves trophoblast invasion, but its pathophysiology is not entirely understood. N6-methyladenosine (m6A) regulators mediate the progression of various cancers. The invasiveness of trophoblast cells is similar to that of tumor cells.

N6-methyladenosine modification in trophoblasts promotes circSETD2 expression, inhibits miR-181a-5p, and elevates MCL1 transcription to reduce apoptosis of trophoblasts.

Preeclampsia (PE) is an obstetric disorder. N6-methyladenosine (m6A) modification is related to PE trophoblast biological behaviors. This study explored the mechanism of m6A-modified circSETD2 in trophoblast biological behaviors.

Membrane attack complexes, endothelial cell activation, and direct allorecognition.

Endothelial cells (ECs) form a critical immune interface regulating both the activation and trafficking of alloreactive T cells. In the setting of solid organ transplantation, donor-derived ECs represent sites where alloreactive T cells encounter major and minor tissue-derived alloantigens. During this initial encounter, ECs may formatively modulate effector responses of these T cells through expression of inflammatory mediators.

RhoGDI1 interacts with PHLDA2, suppresses the proliferation, migration, and invasion of trophoblast cells, and participates in the pathogenesis of preeclampsia.

Preeclampsia (PE) is a pregnancy-associated disease, which is the major cause of mortality on maternity and perinatal infants. It is hypothesized that PE is a consequence of the dysfunction of the trophoblast cells. Pleckstrin homology-like domain, family A, member 2 (PHLDA2) was shown to inhibit the proliferation, migration, and invasion of trophoblast cells in our previous studies.

Effects of Misoprostol on Induction of Labour in Patients with Hypertensive Disorders of Pregnancy: A Meta-Analysis.

Objective: Hypertensive disorders of pregnancy (HDP) can cause serious prenatal and postnatal complications and is a threat to maternal and fetal health. To offer guidance for clinical decisions, we systematically reviewed the effects of misoprostol on induction of labour in HDP patients.

Methods: PubMed, Web of Science, Embase, CNKI, and Wanfang databases were searched for relevant literature from 2010 to 2020.

LncRNA-SNX17 Promotes HTR-8/SVneo Proliferation and Invasion Through miR-517a/IGF-1 in the Placenta of Diabetic Macrosomia.

Gestational diabetes mellitus (GDM) has become a worldwide problem in recent years. Macrosomia, a primary consequence of GDM, has short-term and life-long consequences in the offspring of mothers with GDM. Our previous study showed that miR-517a was dysregulated in placenta and plasma of fetal growth restriction through inhibiting invasion of trophoblast and might be closely related with the regulation of birth weight by the placenta.

Potential of Immune-Related Genes as Biomarkers for Diagnosis and Subtype Classification of Preeclampsia.

Objective: Preeclampsia is the main cause of maternal mortality due to a lack of diagnostic biomarkers and effective prevention and treatment. The immune system plays an important role in the occurrence and development of preeclampsia. This research aimed to identify significant immune-related genes to predict preeclampsia and possible prevention and control methods.

The Role of circRNA-SETD2/miR-519a/PTEN Axis in Fetal Birth Weight through Regulating Trophoblast Proliferation.

Abnormal birth weight is the one of the major causes of adulthood diseases such as obesity, metabolic syndrome, cardiovascular disease, type 2 diabetes, and hypertension. Accumulating evidence has suggested that the placental trophoblast is one of the most important reasons that influence birth weight. Our previous study showed that miR-519a are correlated with low fetal birth weight through regulating trophoblast proliferation.

Circadian clock gene Clock is involved in the pathogenesis of preeclampsia through hypoxia.

Objective: To study the effect of the circadian clock gene Clock on the biological behavior of trophoblasts and its role in the pathogenesis of preeclampsia.

Methods: Quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expression of Clock mRNA. Western blot and immunohistochemistry were used to detect the expression and localization of Clock protein.

Establishing and validating of an laboratory information system-based auto-verification system for biochemical test results in cancer patients.

Background: To establish and validate an laboratory information system (LIS)-based auto-verification (AV) system by using large amounts of biochemical test results in cancer patients.

Methods: An algorithm of the AV process was designed for pre-analysis, analysis, and post-analysis. The limit range check was adjusted three times, while the delta check criteria were first replaced by the same patients' historical extremum results.

YAP Is Decreased in Preeclampsia and Regulates Invasion and Apoptosis of HTR-8/SVneo.

Preeclampsia (PE) is a gestational disorder with hypertension and proteinuria leading to maternal and fetal morbidity and mortality. Yes-associated protein (YAP), a transcription coactivator of Hippo pathway, was identified as an oncoprotein participated in tumorigenesis. However, the effect of YAP on trophoblast has not been investigated.

Altered Expression of miR-518b and miR-519a in the placenta is associated with low fetal birth weight.

Objectives: Previous studies have suggested that the expression and function of placenta-specific microRNAs (miRNAs) are associated with placenta trophoblastic proliferation and invasion. This study investigated whether the altered expression of placenta-specific miRNAs was involved in the development of fetal growth.

Methods: Placenta tissues were obtained from pregnant women with large for gestational age (LGA), intrauterine growth retardation (IUGR), and appropriate for gestational age (AGA) infants (n = 30 in each group).