MicroRNA sequencing of human placentae and matched maternal plasma from 6-23 weeks of gestation
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE151362 | GEO | 2021/12/23
REPOSITORIES: GEO
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Project description:Although recent studies have revealed that microRNAs (miRNAs) regulate fundamental Natural Killer (NK) cell processes including cytotoxicity and cytokine production, little is known about the miRNA-gene regulatory relationships in maternal peripheral blood NK (pNK) cells during pregnancy. To predict the role of miRNAs within gene regulatory networks of maternal pNK cells during pregnancy, we performed comprehensive miRNA and gene expression profiling of maternal pNK cells using a combination of real-time PCR-based array and DNA microarray analyses and analyzed these differential expression levels between first- and third-trimester pNK cells. Furthermore, we constructed regulatory networks for miRNA-mediated gene expression in pNK cells during pregnancy by Ingenuity Pathway Analysis. By PCR-based array analysis of miRNAs, 12 miRNAs including 6 placenta-derived miRNAs [chromosome 19 microRNA cluster (C19MC) miRNAs] were significantly upregulated in third-trimester pNK cells compared to first-trimester pNK cells. pNK cells incorporated C19MC miRNAs, whose interaction would be mediated via exosomes. Rapid clearance of C19MC miRNAs also occurred in NK cells after delivery. By DNA microarray analysis, 13 NK cell function-related genes were significantly downregulated between first- and third-trimester pNK cells. By pathway and network analysis, 9 downregulated NK-function-associated genes were in silico target candidates of 12 upregulated miRNAs including C19MC miRNA miR-512-3p. The results suggest that transfer of placental C19MC-miRNAs into maternal pNK cells occurs during pregnancy. The present study provides clues to understand maternal NK cell functions Gene expressions in human maternal peripheral blood NK cells were measured at 1st-trimester, 3rd-trimester. Five independent experiments were performed at each term (1st-trimester or 3rd-trimester) using different donors for each experiment.
2015-01-13 | E-GEOD-64884 | biostudies-arrayexpress
Project description:Although recent studies have revealed that microRNAs (miRNAs) regulate fundamental Natural Killer (NK) cell processes including cytotoxicity and cytokine production, little is known about the miRNA-gene regulatory relationships in maternal peripheral blood NK (pNK) cells during pregnancy. To predict the role of miRNAs within gene regulatory networks of maternal pNK cells during pregnancy, we performed comprehensive miRNA and gene expression profiling of maternal pNK cells using a combination of real-time PCR-based array and DNA microarray analyses and analyzed these differential expression levels between first- and third-trimester pNK cells. Furthermore, we constructed regulatory networks for miRNA-mediated gene expression in pNK cells during pregnancy by Ingenuity Pathway Analysis. By PCR-based array analysis of miRNAs, 12 miRNAs including 6 placenta-derived miRNAs [chromosome 19 microRNA cluster (C19MC) miRNAs] were significantly upregulated in third-trimester pNK cells compared to first-trimester pNK cells. pNK cells incorporated C19MC miRNAs, whose interaction would be mediated via exosomes. Rapid clearance of C19MC miRNAs also occurred in NK cells after delivery. By DNA microarray analysis, 13 NK cell function-related genes were significantly downregulated between first- and third-trimester pNK cells. By pathway and network analysis, 9 downregulated NK-function-associated genes were in silico target candidates of 12 upregulated miRNAs including C19MC miRNA miR-512-3p. The results suggest that transfer of placental C19MC-miRNAs into maternal pNK cells occurs during pregnancy. The present study provides clues to understand maternal NK cell functions
2015-01-13 | GSE64884 | GEO
Project description:Pancreatic β-cell function impairment is a key mechanism for developing gestational diabetes mellitus (GDM). Maternal and placental exosomes regulate maternal and placental responses during hyperglycemia. Studies have associated exosomal micro RNAs (miRNAs) with GDM development. To date, no studies have been reported that evaluate the profile of miRNAs present in maternal and placental exosomes in the early stages of gestation from pregnancies that develop GDM. We used microarrays to assess whether early pregnancy maternal and placental exosomal miRNA profiles vary according to pancreatic β-cell function in women who will develop GDM (preGDM).
2024-02-29 | GSE243374 | GEO
Project description:Affymetrix miRNA arrays were used to generate miRNA profiles in placenta of Meishan and Yorkshire pigs on stages of initiation (gestational day 26) and establishment (gestational day 50) of placental folds development. The study allowed for the determination of the miRNAs that were differentially expressed in porcine placenta on different gestational day. This study will provide the information to better understanding of the role miRNAs in porcine placental development.
2015-10-01 | GSE62996 | GEO
Project description:Data on the temporal dynamics of human placental gene expression is scarce. We have completed the first whole-genome profiling of human placental gene expression dynamics (GeneChips, Affymetrix®) from early to mid- gestation (10 samples; gestational weeks 5 to 18) and report 154 genes with considerable change in transcript levels (FDR P<0.1). Functional enrichment analysis revealed >200 GO categories that are statistically over-represented among 105 genes with dynamically increasing transcript levels. Analysis in an extended sample (n=43; gestational weeks 5 to 41) conformed a highly significant (FDR P<0.05) expressional peak in mid-gestation placenta for ten genes: BMP5, CCNG2, CDH11, FST, GATM, GPR183, ITGBL1, PLAGL1, SLC16A10, STC1. A central hypothesis of our study states that the aberrant expression of genes characteristic to mid-gestation placenta may contribute to affected fetal growth, maternal preeclampsia (PE) or gestational diabetes (GD). The gene STC1 coding for Stanniocalcin 1 (STC1) was identified with a sharp placental expressional peak in mid-gestation, increased mRNA levels at term and significantly elevated STC1 protein levels in post-partum maternal plasma in all pregnancy complications. The highest STC1 levels were identified in women, who developed simultaneously PE and delivered an SGA baby (median 731 vs 418 pg/ml in controls; P=0.001). CCNG2 and LYPD6 exhibited significantly increased placental mRNA expression and enhanced intensity of immunohistochemistry staining in placental sections all studied in GD and PE cases. Aberrant expression of mid-gestation specific genes in pregnancy complications at term indicates the importance of the fine-scale tuning of the temporal dynamics of transcription regulation in placenta. Observed significantly elevated plasma STC1 in complicated pregnancies warrants further investigations of its potential as a biomarker. Interestingly, a majority of genes with high expression in mid-gestation placenta have also been implicated in adult complex disease. This observation promotes a recently opened discussion on the role of placenta in developmental programming. 4 samples; this submission is extension of our earlier study (accession GSE22490).
2012-05-10 | E-GEOD-37901 | biostudies-arrayexpress
Project description:The placenta regulates maternal-fetal communication, and its defect leads to significant pregnancy complications. The maternal and embryonic circulations are primitively connected in early placentation, but the function of the placenta during this developmentally essential period is relatively unknown. We thus performed a comparative proteomic analysis of the placenta before and after primary placentation and found that the metabolism and transport of lipids were characteristically activated in this period. The placental fatty acid (FA) carriers in specific placental compartments were upregulated according to gestational age, and metabolomic analysis also showed that the placental transport of FAs increased in a time-dependent manner. Further analysis of two mutant mice models with embryonic lethality revealed that lipid-related signatures could reflect the functional state of the placenta. Our findings highlight the importance of the nutrient transport function of the primary placenta in the early gestational period and the role of lipids in embryonic development.
2023-09-06 | PXD026858 | Pride
Project description:Proper functioning of the placenta, the temporary organ crucial in fetal development during pregnancy, is critical for maternal and fetal health. While microRNAs (miRNAs) are known to impact placental gene expression, the effects of other small non-coding RNAs (sncRNAs) on the placental transcriptome are not well-established. Here, we performed small RNA sequencing of 30 chorionic villi samples of varying gestational ages (M = 23.5 ± 11.4 weeks). We observed expression of 1543 sncRNAs, including miRNAs, piRNAs, snRNAs, snoRNAs, and tRNAs, as well as 18,003 miRNA variants (isomiRs), and identified 48 previously-unannotated miRNAs. This novel characterization of the placental sncRNA transcriptome may aid future investigations of sncRNA regulatory functions within the human placenta.
2021-05-14 | GSE164178 | GEO
Project description:Data on the temporal dynamics of human placental gene expression is scarce. We have completed the first whole-genome profiling of human placental gene expression dynamics (GeneChips, Affymetrix®) from early to mid- gestation (10 samples; gestational weeks 5 to 18) and report 154 genes with considerable change in transcript levels (FDR P<0.1). Functional enrichment analysis revealed >200 GO categories that are statistically over-represented among 105 genes with dynamically increasing transcript levels. Analysis in an extended sample (n=43; gestational weeks 5 to 41) conformed a highly significant (FDR P<0.05) expressional peak in mid-gestation placenta for ten genes: BMP5, CCNG2, CDH11, FST, GATM, GPR183, ITGBL1, PLAGL1, SLC16A10, STC1. A central hypothesis of our study states that the aberrant expression of genes characteristic to mid-gestation placenta may contribute to affected fetal growth, maternal preeclampsia (PE) or gestational diabetes (GD). The gene STC1 coding for Stanniocalcin 1 (STC1) was identified with a sharp placental expressional peak in mid-gestation, increased mRNA levels at term and significantly elevated STC1 protein levels in post-partum maternal plasma in all pregnancy complications. The highest STC1 levels were identified in women, who developed simultaneously PE and delivered an SGA baby (median 731 vs 418 pg/ml in controls; P=0.001). CCNG2 and LYPD6 exhibited significantly increased placental mRNA expression and enhanced intensity of immunohistochemistry staining in placental sections all studied in GD and PE cases. Aberrant expression of mid-gestation specific genes in pregnancy complications at term indicates the importance of the fine-scale tuning of the temporal dynamics of transcription regulation in placenta. Observed significantly elevated plasma STC1 in complicated pregnancies warrants further investigations of its potential as a biomarker. Interestingly, a majority of genes with high expression in mid-gestation placenta have also been implicated in adult complex disease. This observation promotes a recently opened discussion on the role of placenta in developmental programming.
2012-05-11 | GSE37901 | GEO
Project description:Background: Maternal iron deficiency (ID) is associated with poor pregnancy and fetal outcomes. The effect is thought to be mediated by the placenta but there is no comprehensive assessment of placental response to maternal ID. Additionally, whether the influence of maternal ID on the placenta differs by fetal sex is unknown. Objectives: Our primary aim was to identify gene and protein signatures of ID mouse placentas at mid-gestation. A secondary objective was to profile the expression of iron genes in mouse placentas across gestation. Methods: We used a real-time PCR based array to determine the mRNA expression of all known iron genes in mouse placentas at embryonic day (E) 12.5, E14.5, E16.5, and E19.5 (n=3 placentas/time point). To determine the effect of maternal ID, we performed RNA sequencing and proteomics in male and female placentas from ID and iron adequate mice at E12.5 (n=8 dams/diet). Results: In female placentas, six genes including transferrin receptor (Tfrc) and solute carrier family 11 member 2 were significantly changed by maternal ID. An additional 154 genes were altered in male ID placentas. Proteomic analysis quantified 7662 proteins in the placenta. Proteins translated from iron responsive element (IRE) containing mRNAs were altered in abundance; ferritin and ferroportin 1 decreased while TFRC increased in ID placenta. Less than 4% of the significantly altered genes in ID placentas occurred both at the transcriptional and translational levels. Conclusions: Our data demonstrate that the impact of maternal ID on placental gene expression in mice is limited in scope and magnitude at mid-gestation. We provide strong evidence for IRE-based transcriptional and translational coordination of iron gene expression in the mouse placenta. Finally, we discover sexually dimorphic effects of maternal ID on placental gene expression, with more genes and pathways altered in male compared with female mouse placentas.
2021-03-12 | PXD023454 | Pride
Project description:Knowing the gene expression profiles of drug-metabolizing enzymes and transporters throughout gestation is important for understanding the mechanisms of pregnancy-induced changes in drug pharmacokinetics. In this study, we compared gene expression of drug-metabolizing enzymes and transporters in the maternal liver, kidney, small intestine, and placenta of pregnant mice throughout gestation by microarray analysis. Specifically, we investigated cytochrome P450 (Cyp), UDP-glucuronosyltranserase (Ugt), and sulfotransferase (Sult), as well as ATP-binding cassette (Abc) and solute carrier (Slc) transporters. We found that relatively few Ugt and Sult genes were impacted by pregnancy in maternal tissues and placenta. Cyp1a2, most Cyp2 isoforms, Cyp3a11, and Cyp3a13 in the liver were down-regulated, with the greatest changes occurring on gestation days (gd) 15 and 19 compared to non-pregnant controls (gd 0). However, Cyp2d40, Cyp3a16, Cyp3a41a, Cyp3a41b, and Cyp3a44 in the liver were induced throughout pregnancy. Cyp expression in mid-gestation placenta (gd 10 and 15) was generally greater than that in term placenta (gd 19). There were also notable changes in Abc and Slc transporters. Abcc3 in the liver was down-regulated by 60%, and Abcb1a, Abcc4, and Slco4c1 in the kidney were down-regulated by 30-60% on gd 15 and 19 versus gd 0. Abcc5 in the placenta was induced 3-fold on gd 10 versus gd 15 and 19, whereas Slc22a3 expression in the placenta on gd 10 was 90% lower than that on gd 15 and 19. Overall, this study demonstrates important gestational age-dependent expression of drug-metabolizing enzymes and transporter genes, which may have mechanistic relevance to human pregnancy. Ninety pregnant mice at gestational days 0, 7.5, 10, 15, and 19 (n = 5-6 per gestational age) were used for the maternal liver, kidney, small intestine and placenta. The placentas were collected on gestational days 10, 15, and 19.
2013-10-08 | E-GEOD-41438 | biostudies-arrayexpress