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Dysregulated lncRNA and mRNA expression in placenta accreta spectrum disorders

ABSTRACT: Dysregulated lncRNA and mRNA expression in placenta accreta spectrum disorders

PROVIDER: PRJNA522355 | ENA |

REPOSITORIES: ENA

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Dysregulated lncRNA and mRNA expression in placenta accreta spectrum disorders

Project description:To find potential biomarkers and molecular mechanism for placenta accreta spectrum disorders , we identified the differently expressed patterns of lncRNAs and mRNAs in invasive placneta and adherent normal placenta tissues. The results provided a novel insight into the pathogenesis of placenta accreta spectrum disorders .

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Discovery of diagnostic biomarker and molecular mechanisms of placenta accreta spectrum

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Project description:This study utilizes advances in single-cell RNA-sequencing to generate transcriptomes from placenta accreta and control specimens.

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RNA sequencing profiling of placental tissues from placenta accreta and control pregnancies

Project description:Placenta accreta is a major cause of maternal morbidity and mortality in modern obstetrics. The study aims to identify the differently expressed lncRNA and mRNA in placenta accreta patients compared with controls and to determine biological pathways, which provides a novel insight ingto thepathogenesis of placneta accreta.

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Placental Accreta Spectrum: Upregulated Cytotrophoblast DOCK4 Contributes to Over Invasion

Project description:In humans, a subset of placental cytotrophoblasts (CTBs) invades the uterus and its vasculature, anchoring the pregnancy and ensuring adequate blood flow to the fetus. Appropriate depth is critical. Shallow invasion increases the risk of pregnancy complications, e.g., severe preeclampsia. Overly deep invasion, the hallmark of placenta accreta spectrum (PAS), increases the risk of pre-term delivery, hemorrhage and death. Previously a rare condition, the incidence of PAS has increased to 1:731 pregnancies, likely due to the rise in uterine surgeries (e.g., Cesarean sections). CTBs track along the scars deep into the myometrium and beyond. Here we compared the global gene expression patterns of CTBs from PAS cases to gestational age-matched control cells that invaded to the normal depth from preterm birth (PTB) deliveries. The mRNA encoding the guanine nucleotide exchange factor, DOCK4, mutations of which promote cancer cell invasion and angiogenesis, was the most highly differentially expressed molecule in PAS samples. Over-expression of DOCK4 increased CTB invasiveness, consistent with the PAS phenotype. Also, this analysis identified other genes with significantly altered expression in this disorder, potential biomarkers. These data suggest that CTBs from PAS cases up regulate a cancer-like pro-invasion mechanism, suggesting molecular as well as phenotypic similarities in the two pathologies.

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Placenta accreta spectrum disorder at single cell resolution: a loss of boundary limits in the uterine endothelium and decidua.

Project description:Objective: The objective of this study is to utilize advances in single-cell RNAsequencing to characterize cellular heterogeneity and transcriptomic signatures of PAS. Our findings can elucidate mechanisms of abnormal placental invasion and identify targets for potential diagnostic and therapeutic biomarkers of PAS. Results: Placental samples from PAS participants and non-PAS cesarean births were included. In total, we analyzed 31,406 individual cells expressing an average of 1,493 genes. Clustering analysis of gene expression identified multiple populations of cells representing syncytiotrophoblasts, cytotrophoblasts, extravillous trophoblasts, decidua,endothelial cells, myeloid, natural killer, and lymphoid cells. When analyzed by disease phenotype, AI showed a unique gene signature most prominently in the endothelial population. The highest expression in AI compared to AO and C was seen in the following genes: DLK1, EGFL6, HGF, APOLD1, and EDNRB. Gene set enrichment analysis of AI endothelial cells identified the following key pathways: blood vessel development, response to growth factors and hormones, regulation of cell adhesion and migration, and pathways in cancer. Conclusions: We present a comprehensive single-cell atlas of PAS across the site of invasion and site of non-adherence. By integrating expression from individual genes per cell, we identified endothelial cells as a key subpopulation in invasive accreta, with expression of genes involved in multiple angiogenic, growth, and mechanical-signaling pathways. After validation, these gene targets may be used to refine diagnostic assays for placenta accreta in early gestation, track disease progression over time, and inform Powered by Editorial Manager® and ProduXion Manager® from Aries Systems Corporation therapeutic discoveries.

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