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Developmental Programming: Impact of prenatal testosterone excess on liver and muscle transcriptome and the relationship between non-coding and coding RNA networks in female sheep [RNA-seq]

ABSTRACT: Developmental Programming: Impact of prenatal testosterone excess on liver and muscle transcriptome and the relationship between non-coding and coding RNA networks in female sheep [RNA-seq]

PROVIDER: PRJNA740325 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14892500.fastq.gz	Fastqsanger.gz
	SRR14892501.fastq.gz	Fastqsanger.gz
	SRR14892502.fastq.gz	Fastqsanger.gz
	SRR14892503.fastq.gz	Fastqsanger.gz
	SRR14892504.fastq.gz	Fastqsanger.gz

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Similar Datasets

Developmental Programming: Impact of prenatal testosterone excess on liver and muscle transcriptome and the relationship between non-coding and coding RNA networks in female sheep [ncRNA-seq]

Project description:This study seeks to assess the effects of prenatal exposure of female sheep to execessive testosterone in metabolically relevant liver and muscle tissue. The goals are to 1) determine noncoding RNA in the control animals and 2) assess the effects of prenatal T-treatment on non-coding RNA. 3) Finally identify putative ncRNA-totalRNA interactions.

2021-10-31 | GSE178775 | GEO

Developmental Programming: Impact of prenatal testosterone excess on liver and muscle transcriptome and the relationship between non-coding and coding RNA networks in female sheep [RNA-seq]

Project description:This study seeks to assess the effects of prenatal exposure of female sheep to execessive testosterone in metabolically relevant liver and muscle tissue. The goals are to 1) determine genes and gene pathways in the control animals and 2) assess the effects of prenatal T-treatment on gene expression and gene pathways. 3) Finally identify putative ncRNA-totalRNA interactions.

2021-10-31 | GSE178774 | GEO

Developmental Programming: adipose depot-specific regulation of non-coding RNAs and their relation to coding RNA expression in prenatal testosterone and prenatal bisphenol-A -treated female sheep

Project description:Inappropriate developmental exposure to steroids is linked to metabolic disorders. Prenatal testosterone excess or bisphenol A (BPA, an environmental estrogen mimic) leads to insulin resistance and adipocyte disruptions in female sheep. Adipocytes are key regulators of insulin sensitivity and tissue-specific differences in insulin sensitivity, coupled with adipose depot-specific changes in key mRNAs, were previously observed. We hypothesized that depot-specific changes in the non-coding RNA (ncRNA) regulators of gene expression would prevail to account for the direction of changes seen in mRNAs. Noncoding RNA (lncRNA, miRNA, snoRNA, snRNA) from various adipose depots of prenatal testosterone and BPA-treated animals were sequenced. Adipose depot-specific changes in the ncRNA that are consistent with the depot-specific mRNA expression in terms of directionality of changes and functional implications in insulin resistance, adipocyte differentiation and cardiac hypertrophy were found. Importantly, the adipose depot-specific ncRNA changes were model-specific that were mutually exclusive suggestive of different regulatory entry points in this regulation.

2024-04-21 | GSE219111 | GEO

Developmental Programming: Impact of prenatal testosterone excess on liver and muscle transcriptome and the relationship between non-coding and coding RNA networks in female sheep

Project description:Developmental Programming: Impact of prenatal testosterone excess on liver and muscle transcriptome and the relationship between non-coding and coding RNA networks in female sheep

| PRJNA740322 | ENA

Developmental Programming: Prenatal Testosterone Excess on Liver and Muscle Coding and Noncoding RNA in Female Sheep.

Project description:Prenatal testosterone (T)-treated female sheep manifest peripheral insulin resistance, ectopic lipid accumulation, and insulin signaling disruption in liver and muscle. This study investigated transcriptional changes and transcriptome signature of prenatal T excess-induced hepatic and muscle-specific metabolic disruptions. Genome-wide coding and noncoding (nc) RNA expression in liver and muscle from 21-month-old prenatal T-treated (T propionate 100 mg intramuscular twice weekly from days 30-90 of gestation; term: 147 days) and control females were compared. Prenatal T (1) induced differential expression of messenger RNAs (mRNAs) in liver (15 down, 17 up) and muscle (66 down, 176 up) (false discovery rate < 0.05, absolute log2 fold change > 0.5); (2) downregulated mitochondrial pathway genes in liver and muscle; (3) downregulated hepatic lipid catabolism and peroxisome proliferator-activated receptor (PPAR) signaling gene pathways; (4) modulated noncoding RNA (ncRNA) metabolic processes gene pathway in muscle; and (5) downregulated 5 uncharacterized long noncoding RNA (lncRNA) in the muscle but no ncRNA changes in the liver. Correlation analysis showed downregulation of lncRNAs LOC114112974 and LOC105607806 was associated with decreased TPK1, and LOC114113790 with increased ZNF470 expression. Orthogonal projections to latent structures discriminant analysis identified mRNAs HADHA and SLC25A45, and microRNAs MIR154A, MIR25, and MIR487B in the liver and ARIH1 and ITCH and miRNAs MIR369, MIR10A, and MIR10B in muscle as potential biomarkers of prenatal T excess. These findings suggest downregulation of mitochondria, lipid catabolism, and PPAR signaling genes in the liver and dysregulation of mitochondrial and ncRNA gene pathways in muscle are contributors of lipotoxic and insulin-resistant hepatic and muscle phenotype. Gestational T excess programming of metabolic dysfunctions involve tissue-specific ncRNA-modulated transcriptional changes.

| S-EPMC8667859 | biostudies-literature

Prenatal programming: adverse cardiac programming by gestational testosterone excess.

Project description:Adverse events during the prenatal and early postnatal period of life are associated with development of cardiovascular disease in adulthood. Prenatal exposure to excess testosterone (T) in sheep induces adverse reproductive and metabolic programming leading to polycystic ovarian syndrome, insulin resistance and hypertension in the female offspring. We hypothesized that prenatal T excess disrupts insulin signaling in the cardiac left ventricle leading to adverse cardiac programming. Left ventricular tissues were obtained from 2-year-old female sheep treated prenatally with T or oil (control) from days 30-90 of gestation. Molecular markers of insulin signaling and cardiac hypertrophy were analyzed. Prenatal T excess increased the gene expression of molecular markers involved in insulin signaling and those associated with cardiac hypertrophy and stress including insulin receptor substrate-1 (IRS-1), phosphatidyl inositol-3 kinase (PI3K), Mammalian target of rapamycin complex 1 (mTORC1), nuclear factor of activated T cells -c3 (NFATc3), and brain natriuretic peptide (BNP) compared to controls. Furthermore, prenatal T excess increased the phosphorylation of PI3K, AKT and mTOR. Myocardial disarray (multifocal) and increase in cardiomyocyte diameter was evident on histological investigation in T-treated females. These findings support adverse left ventricular remodeling by prenatal T excess.

| S-EPMC4916456 | biostudies-literature

Developmental Programming: Impact of prenatal testosterone excess on liver and muscle transcriptome and the relationship between non-coding and coding RNA networks in female sheep [ncRNA-seq]

| PRJNA740327 | ENA

Developmental Programming: Adipose Depot-Specific Transcriptional Regulation by Prenatal Testosterone Excess in a Sheep Model of PCOS

Project description:This study seeks to undertake an assessment of the effects of prenatal exposure of female sheep to excess testosterone, the estrogen precursor, in four different adipose depots. The depots investigated are subcutaneous adipose tissue (SAT) - a fat beneath the skin storing >80% of total body fat in the human body, visceral adipose tissue (VAT) - an intra-abdominal fat primarily associated with digestive system organs, and smaller depots such as epicardial adipose tissue (ECAT) and perirenal adipose tissue (PRAT) that serve specialized functions associated with the organs/tissues in their proximity. The goals are to 1) determine gene expression and gene network profiles in the depots; 2) assess prenatal T-treatment induced disruptions in adipose depot-specific gene expression and gene networks; and 3) identify common and divergent gene and gene pathways underlying depot-specific disruption in prenatal T-treated female sheep.

2020-12-30 | GSE158436 | GEO

Developmental Programming: Impact of prenatal testosterone excess on liver and muscle transcriptome and the relationship between non-coding and coding RNA networks in female sheep

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-10-31 | GSE178777 | GEO

Developmental programming: differential effects of prenatal testosterone excess on insulin target tissues.

Project description:Polycystic ovarian syndrome (PCOS) is the leading cause of infertility in reproductive-aged women with the majority manifesting insulin resistance. To delineate the causes of insulin resistance in women with PCOS, we determined changes in the mRNA expression of insulin receptor (IR) isoforms and members of its signaling pathway in tissues of adult control (n = 7) and prenatal testosterone (T)-treated (n = 6) sheep (100 mg/kg twice a week from d 30-90 of gestation), the reproductive/metabolic characteristics of which are similar to women with PCOS. Findings revealed that prenatal T excess reduced (P < 0.05) expression of IR-B isoform (only isoform detected), insulin receptor substrate-2 (IRS-2), protein kinase B (AKt), peroxisome proliferator-activated receptor-? (PPAR?), hormone-sensitive lipase (HSL), and mammalian target of rapamycin (mTOR) but increased expression of rapamycin-insensitive companion of mTOR (rictor), and eukaryotic initiation factor 4E (eIF4E) in the liver. Prenatal T excess increased (P < 0.05) the IR-A to IR-B isoform ratio and expression of IRS-1, glycogen synthase kinase-3? and -? (GSK-3? and -?), and rictor while reducing ERK1 in muscle. In the adipose tissue, prenatal T excess increased the expression of IRS-2, phosphatidylinositol 3-kinase (PI3K), PPAR?, and mTOR mRNAs. These findings provide evidence that prenatal T excess modulates in a tissue-specific manner the expression levels of several genes involved in mediating insulin action. These changes are consistent with the hypothesis that prenatal T excess disrupts the insulin sensitivity of peripheral tissues, with liver and muscle being insulin resistant and adipose tissue insulin sensitive.

| S-EPMC2954716 | biostudies-literature

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