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ABSTRACT: Genomic binning for AME metagenome

PROVIDER: PRJNA605696 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11058172.fastq.gz	Fastqsanger.gz
	SRR11058173.fastq.gz	Fastqsanger.gz
	SRR11058174.fastq.gz	Fastqsanger.gz
	SRR11058175.fastq.gz	Fastqsanger.gz
	SRR11058176.fastq.gz	Fastqsanger.gz

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Downregulation of miR-192-5p and miR-204-5p in nonclassic apparent mineralocorticoid excess

Project description:The “nonclassic” apparent mineralocorticoid excess (NC-AME) has been identified in approximately 7% of general population. Our aim was to identify miRNAs within urinary exosomes associated to the NC-AME phenotype. A total of 18 urine samples (9 control and 9 NC-AME) derived from adult and children subjects were analyzed using small RNA sequencing.

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Project description:Exposure to adverse early-life environment (AME) increases the incidence of developing adult-onset non-alcoholic fatty liver disease (NAFLD). DNA methylation has been postulated to link AME and late-onset diseases. The objective was to investigate whether and to what extent hepatic DNA methylome was perturbed prior to the development of NAFLD in offspring exposed to AME in mice. AME constituted maternal western diet and late-gestational stress. Male offspring livers at birth (d0) and weaning (d21) were used for evaluating DNA methylome and transcriptome using reduced representation of bisulfite sequencing and RNA-seq, respectively. We found AME caused 5,879 differentially methylated regions (DMRs) and zero differentially expressed gene (DEG) at d0, and 2,970 and 123, respectively at d21. Majority of the DMRs were distal from gene transcription start sites and did not correlate with DEGs. The DEGs at d21 were significantly en-riched in GO biological processes characteristic of liver metabolic functions. In conclusion, AME drove changes in hepatic DNA methylome which preceded perturbations in the hepatic metabolic transcriptome, which preceded the onset of NAFLD. We speculate that subtle impacts in dynamic enhancers lead to long-range regulatory changes that manifest over time as gene network alter-nations to increase the incidence of NAFLD later in life.

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