Ontology highlight
ABSTRACT:
PROVIDER: PRJNA706741 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13859601.fastq.gz | Fastqsanger.gz | |||
| SRR13859602.fastq.gz | Fastqsanger.gz | |||
| SRR13859603.fastq.gz | Fastqsanger.gz | |||
| SRR13859604.fastq.gz | Fastqsanger.gz | |||
| SRR13859605.fastq.gz | Fastqsanger.gz |
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Project description:Exosomes are membranous extracellular vesicles 50–100 nm in size and are involved in cellular communication via the delivery of proteins, lipids, and RNAs. Emerging evidence shows that exosomes play a critical role in cancer. A recent study has revealed that maternal and umbilical cord serum-derived exosomes may enhance endothelial cell proliferation and migration. However, the role of exosomes isolated from the human umbilical cord in cancer development has not been investigated. To explore the potential differences in the composition and function of proteins from umbilical cord blood exosomes and maternal serum exosomes, we conducted a proteomic analysis of exosomes by mass spectrometry and bioinformatics analysis. We used the CCK-8 assay and flow cytometry to study the biological effects of umbilical serum exosomes on hepatoma cells. Our study shows that umbilical cord blood is enriched with proteins involved in ECM-receptor interactions, which may be closely related to cell metastasis and proliferation. Our findings indicate that exosomes derived from human umbilical serum can suppress the viability of hepatoma cells and may induce apoptosis of hepatoma cells. This evidence suggests that umbilical cord serum-derived exosomes may be potential leads for the development of biotherapy for liver cancer.
2022-02-17 | PXD025079 | Pride
Project description:Preeclampsia (PE) is a peculiar multisystemic disorder that contributes to maternal and perinatal morbidity. Exosomes, existing in the circulation, origin from late endosomes which are secreted into the extracellular surrounding by diverse cell types under different conditions, can mediate intercellular communication via transporting its constituents and regulate inflammation, immunomodulation and angiogenesis. We hypothesize that exosomes from trophoblast in preeclampsia complications under pathological hypoxia microenvironment impair vascular development by transmitting its contents to endothelial cells. Here, transwell and tube formation assays revealed that exosomes from hypoxic trophoblast cells attenuated the migration, and tube formation in human umbilical vein endothelial cells (HUVECs) in vitro. In a mouse model, hypoxic trophoblast cells derived exosomes leaded to vascular dysfunction and caused adverse PE-like birth outcomes. Next, we detected lncRNA expression in cord blood plasma derived exosomes from gestational age-matched preeclampsia and normal pregnancies by microarray analysis. Then, we identified the possible mechanisms of one up-regulated exosomal lncRNA, TINCR. Application of Quantitative RT-PCR, lncTINCR was confirmed overexpressing in exosomes released from cord blood plasma, peripheral blood plasma and human placental trophoblasts of preeclampsia patients. Moreover, the exosomal lncTINCR could be specifically secreted by hypoxic trophoblast cells and transferred to HUVECs, which increased autophagy in HUVECs and impaired angiogenesis of endothelial cells in vitro. Furthermore, we demonstrated that lncTINCR was considered as a competing endogenous RNA to regulate miR-424, which resulted in elevated ATG5 expression. Thus, we reported that exosomes intervened effective delivering of lncTINCR to endothelial cells to damage vascular functions and result in the development of PE. The newly identified exosomal lncTINCR /miR-424/ATG5 axis may present potential novel targets of diagnosis and treatment for PE. lncRNA profiles of cord blood plasma derived exosomes from gestational age-matched preeclampsia and normal pregnancies
2024-09-02 | GSE183466 | GEO
Project description:Preeclampsia (PE) is characterized by new-onset hypertension after 20 weeks of pregnancy and results in high maternal and fetal mortality worldwide. It has been reported that PE is associated with abnormalities in the umbilical cord and cord blood. However, previous studies were focused primarily on the transcriptomics level, while the underlying gene regulatory landscapes are still unclear. Thus, we performed the Assay for Transposase-Accessible Chromatin with high-throughput sequencing (ATAC-seq) using the umbilical cord blood samples collected from a patient with superimposed PE and three healthy donors to uncover the chromatin accessibility changes attributed to PE. We have identified genes associated with immunomodulation and hypoxia response that have higher chromatin accessibility close to their transcription start sites. Motif analysis indicated that the GATA family transcription factor binding was enriched in PE and may play an essential regulatory role in the disease progression. Overall, our findings provide an overview of gene regulatory programs and the corresponding downstream pathways associated with PE that may influence the placenta function and fetal growth.
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Project description:Introduction. Preeclampsia (PE) carries increased risks of cardiovascular- and metabolic diseases in mothers and offspring during the life course. While the severe early-onset PE (EOPE) phenotype originates from impaired placentation in early pregnancy, late-onset PE (LOPE) is in particular associated with pre-existing maternal cardiovascular- and metabolic risk factors. We hypothesize that PE is associated with altered epigenetic programming of placental and fetal tissues and that these epigenetic changes might elucidate the increased cardiovascular- and metabolic disease susceptibility in PE offspring. Methods. A nested case-control study was conducted in The Rotterdam Periconceptional Cohort comprising 13 EOPE, 16 LOPE, and three control groups of 36 uncomplicated pregnancies, 27 normotensive fetal growth restricted (FGR) and 20 normotensive preterm birth (PTB) complicated pregnancies. Placental tissue, newborn umbilical cord blood leucocytes (UC-WBC) and umbilical vein endothelial cells (HUVEC) were collected and DNA methylation of cytosine-guanine dinucleotides was measured by the Illumina HumanMethylation450K BeadChip. An epigenome-wide analysis was performed by using multiple linear regression models. Results. Epigenome-wide tissue-specific analysis between EOPE and PTB controls revealed 5001 mostly hypermethylated differentially methylated positions (DMPs) in UC-WBC and 869 mostly hypomethylated DMPs in placental tissue, situated in or close to genes associated with cardiovascular-metabolic developmental pathways. Discussion. This study shows differential methylation in UC-WBC and placental tissue in EOPE as compared to PTB, identifying DMPs that are associated with cardiovascular system pathways. Future studies should examine these loci and pathways in more detail to elucidate the associations between prenatal PE exposure and the cardiovascular disease risk in offspring.
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Project description:Premature infants have a high risk of bronchopulmonary dysplasia (BPD), which is characterized by abnormal development of alveoli and pulmonary vessels. Exosomes and exosomal miRNAs (EXO-miRNAs) from bronchoalveolar lavage fluid are involved in the development of BPD and might serve as predictive biomarkers for BPD. However, the roles of exosomes and EXO-miRNAs from umbilical cord blood of BPD infants in regulating angiogenesis are yet to be elucidated. In this study, we showed that umbilical cord blood-derived exosomes from BPD infants impaired angiogenesis in vitro. Next generation sequencing of EXO-miRNAs from preterm infants without (NBPD group) or with BPD (BPD group) uncovered a total of 418 differentially expressed (DE) EXO-miRNAs. These DE EXO-miRNAs were primarily enriched in cellular function-associated pathways including the PI3K/Akt and angiogenesis- related signaling pathways. Among those EXO-miRNAs which are associated with PI3K/Akt and angiogenesis-related signaling pathways, BPD reduced expression of hsa-miR-103a-3p and hsa-miR-185-5p exhibiting most significant reduction (14.3% and 23.1% of NBPD group, respectively); BPD increased hsa-miR-200a-3p expression by 2.64 folds of NBPD group. Furthermore, overexpression of hsa-miR-103a-3p and hsa-miR-185-5p in normal human umbilical vein endothelial cells (HUVECs) significantly enhanced endothelial cell proliferation, tube formation and cell migration, whereas overexpressing hsa-miR-200a-3p inhibited these cellular responses. This study demonstrates that exosomes derived from umbilical cord blood of BPD infants impair angiogenesis, possibly via DE EXO-miRNAs, which might contribute to the development of BPD.
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Project description:Human reticulocytes were enriched from human umbilical blood, and cultured in vitro for the production of reticulocyte-derived exosomes (HuRex)to unveil their proteomic composition. As research on the molecular-cargo of exosomes is largely confounded by the lack of a “gold-standard” methodology, we applied several approaches for obtaining HuRex prior to MS. HuRex preparations were obtained from cultures in absence of serum (AS) from three donors and isolated by means of size-exclusion chromatography (SEC) (n=3) and ultracentrifugation (UC) (n=3). HuRex preparations in the presence of serum were obtained from three other donors and purified by SEC (n=3) and UC (n=1).
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Project description:We used microarray technology to establish the differential RNA expression profiles in umbilical cord blood exosomes from preeclampsia patients compared with normal controls.
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Project description:Fiber diet plays a beneficial role in neurocognitive disorders, like dementia and Alzheimer’s Disease. However, insufficient fiber consumption in public increases the concern about public health, particularly about neurocognitive diseases. To survey the association between fiber dietary and neurocognitive performances, mice were subjected to normal-fiber diet or low-fiber diet during gestation, and the neurocognitive functions of the offspring were assessed. We found that maternal low-fiber diet impaired the cognitive functions, and the impairments can be reversed by butyrate, rather than propionate intake. Mechanism studies showed that HDAC4 might become the most potential mediator in butyrate-dependent neurocognitive improvement. Besides, using human maternal serum and paired umbilical cord blood samples, we demonstrated that the SCFA levels in offspring are positively correlated with levels in maternal serum. Those results provide a solid basis for not only maternal fiber diet regulates neurocognitive functions in offspring through altering SCFA levels, but clinical practice in SCFAs-dependent maternal intervention for offspring health.
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