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MiRNAs expression in human placental tissue with Hemoglobin Bart's Hydrops Fetalis Syndrome

ABSTRACT: MiRNAs expression in human placental tissue with Hemoglobin Bart's Hydrops Fetalis Syndrome

PROVIDER: PRJNA767050 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16100857.fastq.gz	Fastqsanger.gz
	SRR16100858.fastq.gz	Fastqsanger.gz
	SRR16100859.fastq.gz	Fastqsanger.gz
	SRR16100860.fastq.gz	Fastqsanger.gz
	SRR16100861.fastq.gz	Fastqsanger.gz

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MiRNAs expression in human placental tissue with Hemoglobin Bart's Hydrops Fetalis Syndrome

Project description:Hemoglobin Bart’s hydrops fetalis syndrome (BHFS) is the most severe form of α-thalassemia. Histological alternations can be observed in placenta, but placental transcriptome profile and circular RNAs have not been study in this disease. The aim of this study was to define the placental transcriptional changes and find relevant circular RNAs in BHFS. We performed high-throughput RNA sequencing to detect placental samples from fetuses affected by BHFS (n=5) and normal fetuses (NF, n=5). Our results showed 152 differentially expressed genes (DEGs), 112 circRNAs, and 45 microRNAs that were differentially expressed. DEGs were found to be involved in Gene Ontology terms related to gas transport, cell adhesion, oxidative stress, organ development, hemopoiesis, etc. Our study characterized the placental transcriptome of BHFS.

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MRNAs and non-coding RNAs expression in human placental tissue with Hemoglobin Bart's Hydrops Fetalis Syndrome

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RNA expression in human placental tissue with Hemoglobin Bart's Hydrops Fetalis Syndrome

Project description:RNA expression in human placental tissue with Hemoglobin Bart's Hydrops Fetalis Syndrome

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MRNAs and non-coding RNAs expression in human placental tissue with Hemoglobin Bart's Hydrops Fetalis Syndrome

Project description:MRNAs and non-coding RNAs expression in human placental tissue with Hemoglobin Bart's Hydrops Fetalis Syndrome

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Let-7 miRNAs repress HIC2 to regulate BCL11A transcription and hemoglobin switching [RNA-Seq]

Project description:The fetal hemoglobin (HBG) regulator BCL11A is repressed by HIC2 to regulate hemoglobin switching. HIC2 itself is under developmental control, highly expressed in fetal tissues and decreased in adult cells, but the mechanism of this developmental regulation is unclear. Here, we demonstrate that HIC2 is developmentally controlled by miRNAs, and loss of global miRNA biogenesis through DICER1 depletion leads to upregulation of HIC2 and HBG. We subsequently identify the adult-expressed let-7 miRNA family as a repressor of HIC2 expression. Ectopic expression of let-7 in fetal-type cells repressed HIC2 levels, while let-7 inhibition in adult erythroblasts upregulated HIC2 levels. Let-7 regulates BCL11A and HBG through induction of HIC2 and reduction of GATA1 binding at the BCL11A erythroid enhancer. Finally, HIC2 depletion rescues BCL11A-mediated repression of fetal hemoglobin in let-7 inhibited cells. Together these data demonstrate a key miRNA-mediated mechanism for developmental regulation of BCL11A expression and fetal hemoglobin repression in adult erythroid cells.

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Let-7 miRNAs repress HIC2 to regulate BCL11A transcription and hemoglobin switching [ChIP-Seq]

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Let-7 miRNAs repress HIC2 to regulate BCL11A transcription and hemoglobin switching [Capture-C]

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Let-7 miRNAs repress HIC2 to regulate BCL11A transcription and hemoglobin switching [ATAC-Seq]

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Transgenic expression of human C19MC miRNAs impacts placental morphogenesis

Project description:Transgenic expression of human C19MC miRNAs impacts placental morphogenesis

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microRNA expression profiles of reticulocytes for hereditary persistence of fetal hemoglobin and β-thalssemia minor with high fetal hemoglobin.

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