Cell-type specific distribution and activation of type I IFN pathway molecules at the placental maternal-fetal interface in response to COVID-19 infection.

Background And Objective: COVID-19 infection in pregnancy significantly increases risks of adverse pregnancy outcomes. However, little is known how the innate immunity at the placental maternal-fetal interface responds to COVID-19 infection. Type I IFN cytokines are recognized as a key component of the innate immune response against viral infection.

Downregulation of miR-126-3p expression contributes to increased inflammatory response in placental trophoblasts in preeclampsia.

MiR-126-3p is a prototype of an endothelial miRNA and has protective effects on endothelial cells. However, little is known about the effects of miR-126-3p on placental trophoblasts. In the present study, we tested the hypothesis that aberrant miR-126-3p expression is present in preeclamptic placenta which contributes to increased inflammatory response in trophoblasts.

Prolonged Fetal Heart Rate Decelerations in Labor: Can We Reduce Unplanned Primary Cesarean Sections in This Group?

Introduction: Non-reassuring fetal tracing is the second leading cause of primary cesarean delivery in the United States. Prolonged fetal heart rate decelerations are non-reassuring fetal heart rate characteristics, which do not uniformly predict poor fetal outcome but can prompt obstetricians to proceed with cesarean delivery. The objective of this manuscript is to identify a strategy to reduce the primary cesarean section rate in patients with prolonged fetal heart rate decelerations in labor.

Upregulation of histone H3K9 methylation in fetal endothelial cells from preeclamptic pregnancies.

Adverse intrauterine environment has been considered a predisposing factor for fetal programming in preeclampsia. Using human umbilical vein endothelial cells (HUVECs), we specifically explored if aberrant histone methylation occurs in fetal endothelial cells in preeclampsia. Strikingly, we found that increased di-, and tri-methylation of histone H3 lysine 9 (H3K9me2 and H3K9me3) expression were associated with upregulation of methyltransferase G9a and downregulation of endothelial nitric oxide synthase and CuZn-SOD expression in preeclamptic HUVECs.

Maternal soluble PD-1 levels are significantly increased in women with preeclampsia.

Problem: Programmed cell death-1 (PD-1) and its ligand (PD-L1) have emerged as key players in regulating immune tolerance. Preeclampsia is associated with maladaptation of immune tolerance during pregnancy. This study aimed to determine if maternal soluble PD-1 (sPD-1) and soluble PD-L1 (sPD-L1) levels are altered in preeclampsia.

Downregulation of vitamin D receptor and miR-126-3p expression contributes to increased endothelial inflammatory response in preeclampsia.

Problem: To investigate whether downregulation of miR-126-3p and vitamin D receptor (VDR) expression contributes to increased endothelial inflammatory response in preeclampsia.

Methods Of Study: Maternal vessel miR-126-3p expression was assessed by in situ hybridization. VDR expression and VCAM-1 expression were determined by immunostaining.

Aberrant pro-atrial natriuretic peptide/corin/natriuretic peptide receptor signaling is present in maternal vascular endothelium in preeclampsia.

Objective: Corin is a serine protease that converts pro-atrial natriuretic peptide (pro-ANP) to atrial natriuretic peptide (ANP), a cardiac hormone that regulates salt-water balance and blood pressure. ANP is degraded by natriuretic peptide receptor (NPR). This study was to determine if aberrant pro-ANP/corin/NPR signaling is present in maternal vascular system in preeclampsia.