Dataset Information

Distinct communication patterns of trophoblastic miRNA among the maternal-placental-fetal compartments.

ABSTRACT: INTRODUCTION:The placenta produces microRNAs (miRNA) that may traffic to the maternal or fetal compartments and influence the physiology of pregnancy. The trafficking patterns of miRNA expressed from the large human chromosome 19 and chromosome 14 clusters (C19MC and C14MC), remains unclear. We interrogated the cross-sectional landscape of miRNA expression within the human placenta, fetal and maternal plasma to elucidate miRNA trafficking. We hypothesized that C19MC and C14MC miRNAs have similar expression patterns across the maternal-fetal compartments. METHODS:Placental biopsies, maternal and fetal venous plasma were collected from 25 pregnancies, and RNA was quantified using next generation sequencing. We identified expression and correlations differences among the compartments, and uncovered distinct miRNA expression patterns using consensus clustering. RESULTS:We found that the placenta exhibits the highest total abundance, average miRNA expression and lowest variance of both C19MC and C14MC miRNAs. The C19MC miRNAs had a comparable expression and variance in fetal and maternal plasma and higher expression in the placenta. In contrast, the C14MC miRNAs had comparable expression between the placenta and fetal plasma, which was higher than the maternal plasma. We also identified 5 distinct groups of trophoblastic miRNAs with different expression patterns in each compartment. DISCUSSION:This is the first comprehensive analysis of C19MC and C14MC miRNA expression patterns in the human placental, maternal and fetal compartments. Our findings suggest that C14MC miRNAs are produced by both the fetus and placenta, but C19MC miRNAs are produced primarily in the placenta and are trafficked to the fetal and maternal compartments.

SUBMITTER: Paquette AG

PROVIDER: S-EPMC6329371 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature

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Distinct communication patterns of trophoblastic miRNA among the maternal-placental-fetal compartments.

Paquette Alison G AG Chu Tianjiao T Wu Xiaogang X Wang Kai K Price Nathan D ND Sadovsky Yoel Y

Placenta 20181022

<h4>Introduction</h4>The placenta produces microRNAs (miRNA) that may traffic to the maternal or fetal compartments and influence the physiology of pregnancy. The trafficking patterns of miRNA expressed from the large human chromosome 19 and chromosome 14 clusters (C19MC and C14MC), remains unclear. We interrogated the cross-sectional landscape of miRNA expression within the human placenta, fetal and maternal plasma to elucidate miRNA trafficking. We hypothesized that C19MC and C14MC miRNAs have ...[more]

PMID: 30501878

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Project description:OBJECTIVE:To examine inflammatory mediators in three fetomaternal biological compartments to inform theory related to the fetal and maternal inflammatory contributions to parturition at term and preterm. METHODS:We conducted a cross-sectional study of amniotic fluid, cord blood, and maternal plasma from women with singleton pregnancies. Women had one of four conditions: term labor (n=11), term not in labor (n=13), spontaneous preterm birth with intact membranes (preterm birth; n=13), or preterm prelabor rupture of membranes (PROM; n=8). We measured two damage-associated molecular pattern markers (high-mobility group box-1 [HMGB1] and uric acid) and two acute phase response markers (interleukin [IL]-6 and C-reactive protein [CRP]) using enzyme-linked immunosorbent assay. The distribution of each analyte within amniotic fluid, cord blood, and maternal plasma across the four conditions (term not in labor, term labor, preterm birth, and preterm PROM) were calculated. To explore whether there were distributional differences in each analyte across each of the four labor conditions, we used a nonparametric Kruskal-Wallis test. For analytes that differed across groups, we further compared distributions by labor group (term labor vs term not in labor, and preterm PROM vs preterm birth). RESULTS:Fetal compartments (amniotic fluid and cord blood) showed higher HMGB1 in term labor vs term not in labor and preterm PROM vs preterm birth. Amniotic fluid IL-6, cord blood CRP and cord blood uric acid were higher in term vs term not in labor. Cord blood uric acid was higher in preterm PROM vs preterm birth. Only maternal plasma IL-6 was higher in term labor vs term not in labor. CONCLUSION:Accumulation of HMGB1 and an overall increase in inflammation observed on the fetal side, but not the maternal side, may be signals of parturition. Understanding fetal-derived proparturition inflammatory signals at term and preterm, especially in preterm PROM, might provide fetal-specific biomarkers and identify underlying mechanisms and targets for interventions to reduce the risk of preterm birth and preterm PROM.

Project description:Fetal placental macrophages and microglia (resident brain macrophages) have a common origin in the fetal yolk sac. Yolk-sac-derived macrophages comprise the permanent pool of brain microglia throughout an individual's lifetime. Inappropriate fetal microglial priming may therefore have lifelong neurodevelopmental consequences, but direct evaluation of microglial function in a living fetus or neonate is impossible. We sought to test the hypothesis that maternal obesity would prime both placental macrophages and fetal brain microglia to overrespond to an immune challenge, thus providing a window into microglial function using placental cells. Obesity was induced in C57BL/6?J mice using a 60% high-fat diet. On embryonic day 17.5, fetal brain microglia and corresponding CD11b?+?placental cells were isolated from fresh tissue. Cells were treated with media or lipopolysaccharide (LPS). Tumor necrosis factor-alpha (TNF-?) production by stimulated and unstimulated cells was quantified via ELISA. We demonstrate for the first time that the proinflammatory cytokine production of CD11b?+?placental cells is strongly correlated with that of brain microglia (Spearman's ??=?0.73, p?=?0.002) in the setting of maternal obesity. Maternal obesity-exposed CD11b?+?cells had an exaggerated response to LPS compared to controls, with a 5.1-fold increase in TNF-? production in placentas (p?=?0.003) and 3.8-fold increase in TNF-? production in brains (p?=?0.002). In sex-stratified analyses, only male obesity-exposed brains and placentas had significant increase in TNF-? production in response to LPS. Taken together, these data suggest that maternal obesity primes both placental macrophages and fetal brain microglia to overproduce a proinflammatory cytokine in response to immune challenge. Male brain and placental immune response is more marked than female in this setting. Given that fetal microglial priming may impact neuroimmune function throughout the lifespan, these data could provide insight into the male predominance of certain neurodevelopmental morbidities linked to maternal obesity, including cognitive dysfunction, autism spectrum disorder, and ADHD. Placental CD11b+ macrophages may have the potential to serve as an accessible biomarker of aberrant fetal brain immune activation in maternal obesity. This finding may have broader implications for assaying the impact of other maternal exposures on fetal brain development.

Dataset Information

Distinct communication patterns of trophoblastic miRNA among the maternal-placental-fetal compartments.

Publications

Distinct communication patterns of trophoblastic miRNA among the maternal-placental-fetal compartments.

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