Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

42 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dietary alleviation of malprogramming across generations: metabolic, transcriptional, and epigenetic signatures of increased resistance to an obesogenic diet in mice

ABSTRACT: We have previously reported that providing a control diet to obese and diabetic mice during the periconceptional/gestation/lactation period, led to a drastic sex-specific shift from susceptibility to resistance to high fat feeding (HFD) in the female offspring. In the present study, we aimed to characterize exhaustively the metabolic phenotype of F1 and F2 sensitive (S1, S2) and resistant (R1, R2) mice and underscore in the liver, muscle and adipose tissue, the transcriptional and epigenetic mechanisms supporting the response to HFD, the trait of resistance/susceptibility and the adaptation across generations. We report the transcriptomic analyses realized based on a candidate gene approach in the liver using a custom mouse microchip. A direct comparison strategy with dye-swapping was used to compare two conditions and dye-swaps were replicated several times with at least 4 different animals/group. The comparisons of primary interest: S1 vs N1 (S1/N1); S2 vs N2 (S2/N2); R2 vs N2 (R2/N2); R2 vs S2 (R2/S2) and S2 vs S1 (S2/S1) were made according to a design such that secondary comparisons could be estimated.

ORGANISM(S): Mus musculus

SUBMITTER: Jean-Philippe Jais

PROVIDER: E-GEOD-30085 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

SARS-CoV-2 S protein ACE2 interaction reveals novel allosteric targets

Project description:SARS-CoV-2 spike protein binding to receptor ACE2 allosterically enhances furin proteolysisat distal S1/S2 cleavage sites

2021-08-09 | PXD023138 | Pride

Red blood cells from mice on high fat diet induce macrophage activation during phagocytosis

Project description:We studied macrophage gene expression from mice fed chow diet (C) or 60% high fat diet (HF), that phagocytized C-RBC, HFD-RBC, or no RBC. Macrophages from mice on HF diet were activated toward a pro-inflammatory phenotype. In macrophages isolated from CD mice, RBC phagocytosis yielded a gene expression pattern similar to HF macrophages. Incubation of HF-RBC with macrophages resulted in a significantly more pronounced upregulation of pro-inflammatory chemokines as compared to C-RBC. Peritoneal macrophages were obtained from C57BL/6 mice fed either C or HF diet. Phagocytosis was performed in vitro with C-RBC or HF-RBC; macrophages not exposed to RBC served as a control. Affymetrix Mouse Gene 1.0 ST microarray chips were used to assess the gene expression profile.

2013-08-28 | E-GEOD-50240 | biostudies-arrayexpress

Methylome analysis of epiRIL344 BC1-S1 to BC1-S6 aerial part

Project description:DNA methylation profiling in epiRIL344 BC1-S1 to BC1-S6 aerial part (epiRIL344_BC1-S1 - epiRIL344_BC1-S2 - epiRIL344_BC1-S3 - epiRIL344_BC1-S4 - epiRIL344_BC1-S5 - epiRIL344_BC1-S6) Keywords: Genome binding/occupancy profiling by genome tiling array

2012-09-03 | GSE37285 | GEO

Transcriptome Analysis of Exercise Ancestry

Project description:Transcriptome analysis of gastrocnemius muscle RNA samples from exercise and sedentary ancestries Early life and pre-conception environmental stimuli can affect adult health-related phenotypes. Exercise training is an environmental stimulus affecting many systems throughout the body and appears to alter offspring phenotypes. The aim of this study was to examine the influence of parental exercise training, or M-bM-^@M-^\exercise ancestry,M-bM-^@M-^] on morphological and metabolic phenotypes in multiple generations of mouse offspring. F0 C57BL/6 mice were exposed to voluntary exercise or sedentary lifestyle and bred with like-exposed mates to produce an F1 generation. F1 mice of both ancestries were sedentary and sacrificed at 8 wk or bred with littermates to produce an F2 generation, which was also sedentary and sacrificed at 8 wk. Small, but broad generation- and sex-specific effects of exercise ancestry were observed for body mass, fat and muscle mass, serum insulin, glucose tolerance, and muscle gene expression. F1 EX females were heavier than F1 SED females, but F1 SED females had higher absolute tibialis anterior and omental fat masses. Serum insulin was lower in F1 SED females compared to F1 EX females. F2 EX females had impaired glucose tolerance compared to F2 SED females. Analysis of skeletal muscle mRNA levels revealed several generation- and sex-specific differences in mRNA levels for multiple genes, especially those related to metabolic genes (e.g., F1 EX males had lower mRNA levels of Hk2, Ppard, Ppargc1M-NM-1, Adipoq, and Scd1 than F1 SED males). These results provide preliminary evidence that parental exercise training can influence health-related phenotypes in mouse offspring. We analyzed RNA from 10 males each from exercise and sedentary ancestries over 2 generations of offspring (F1 and F2)

2012-08-30 | E-GEOD-40469 | biostudies-arrayexpress

Dietary alleviation of maternal obesity and diabetes: increased resistance to diet-induced obesity transcriptional and epigenetic signatures

Project description:We have previously reported that providing a control diet to obese and diabetic mice during the periconceptional/gestation/lactation period, led to a drastic sex-specific shift from susceptibility to resistance to high fat feeding (HFD) in the female offspring. In the present study, we aimed to characterize exhaustively the metabolic phenotype of F1 and F2 sensitive (S1, S2) and resistant (R1, R2) mice and underscore in the liver, muscle and adipose tissue, the transcriptional and epigenetic mechanisms supporting the response to HFD, the trait of resistance/susceptibility and the adaptation across generations. We report the transcriptomic analyses realized based on a candidate gene approach in the liver using a custom mouse microchip.

2012-04-01 | GSE30085 | GEO

Gene expression in liver and lung of a high-fat diet fed, metastasizing mammary tumor-bearing and obesity-resistant mice

Project description:We explored early changes in gene expression in the livers and lungs of the HFD-fed, metastasizing mammary tumor-bearing and obesity-resistant mice mice. These alterations may have led to favorable conditions for both the formation of pro-inflammatory and pro-mitotic microenvironments in the target organs that promote immune cell infiltration and differentiation, as well as infiltration and proliferation of metastatic tumor cells. Total RNA was isolated from hepatic and pulmonary tissues of high fat diet fed-4T1 cell-injected mice or high fat diet fed-sham mice. Gene expressions were compared to control diet fed-same conditional mice.

2012-03-05 | E-GEOD-36211 | biostudies-arrayexpress

miR-122-dependent binding of TNRC6 to HCV RNA

Project description:The liver-specific microRNA, miR-122, is an essential host factor for replication of hepatitis C virus (HCV), an important infectious cause of chronic liver disease and hepatocellular carcinoma. miR-122 stabilizes the positive-strand HCV RNA genome and promotes viral RNA synthesis by binding two closely spaced sites (S1 and S2) near the 5’ end of the genome in association with Ago2. Ago2 is essential for both host factor activities, but whether other host proteins are involved is unknown. Using a quantitative proteomics approach, we identified TNRC6A (GW182) and its paralogs (TNRC6B and TNRC6C), as functionally important components of the miR-122/Ago2 host factor complex binding HCV RNA. Depletion of any two TNRC6 proteins reduced HCV replication in Huh-7.5 cells,but did not reduce viral RNA stability or translational activity, but rather dampened miR-122 stimulation of viral RNA synthesis. However, TNRC6 depletion had no effect on replication of HCV in which S2 was mutated so that miR-122 binds only S1, whereas it significantly enhanced replication when S1 was mutated and only S2 bound by miR-122. Consistent with this, we found that TNRC6 proteins preferentially associate with the S1 site, and that the association of Ago2 with S2 is increased in TNRC6-depleted cells. Collectively, these data suggest a model in which TNRC6 proteins, which are known to interact with Ago2, preferentially direct the miR-122/Ago2 complex to S1 while restricting its association with S2, thereby fine tuning the spatial organization of miR-122/Ago2 complexes bound to the viral RNA.

2019-04-24 | PXD013054 | Pride

Cerebrospinal Fluid-Derived Microvesicles from Sleeping Sickness Patients Alter Protein Expression in Human Astrocytes

Project description:Human African trypanosomiasis (HAT) caused by the extracellular protozoon Trypanosoma brucei, is a neglected tropical disease affecting the poorest communities in sub-Saharan Africa. HAT progresses from a hemolymphatic first stage (S1) to a meningo-encephalitic late stage (S2) when parasites reach the central nervous system, although the existence of an intermediate stage (Int.) has also been proposed. The pathophysiological mechanisms associated with the development of S2 encephalopathy are yet to be fully elucidated. In the present study, we used data independent acquisition mass spectrometry (DIA-MS) to investigate the potential pathogenic effects of microvesicles (MVs) derived from HAT patients’ cerebrospinal fluid (CSF). To assess potential biological properties of these MVs, immortalized human astrocytes were exposed, in vitro, to MVs enriched from S1, Int. or S2 CSF. DIA-MS analyses showed that S2 MVs induced, compared to Int. or S1 MVs, a stronger proteome modulation in astrocytes that resembled the one produced by IFN-γ, a key molecule in HAT pathogenesis. Our results indicate that HAT S2 CSF harbors MVs potentially involved in the mechanisms of pathology associated with HAT late stage. Such vesicles might thus represent a new player to consider in future functional studies.

2019-10-28 | PXD014945 | Pride

Proteomics changes associated with the development of açaí (Euterpe oleracea Mart.) seeds

Project description:In addition to being a source of polyphenols with beneficial health properties, açaí seeds are a rich source of mannans, which can be used to generate bioethanol or be converted to high-value D-mannose. Here we present a quantitative proteome dataset of açaí seeds at four stages of development (S1, S2, S3 and S4 stages), in which 2465 high confidence proteins were identified and 524 of them show statistically different abundance profiles during development. Several enzymes involved in the biosynthesis of nucleotide-sugars were quantified, especially those dedicated to the formation of GDP-mannose, which showed an increase in abundance between stages S1 and S3. Our data suggest that linear mannans present in high amounts in the cell walls of the endosperm of mature seeds are primarily deposited as galactomannans and during development they lose their galactosyl groups by alpha-galactosidase activity, which show increased abundances in the S3 and S4 stages. Additionally, we quantified the enzymes participating in the central pathway of flavonoid biosynthesis responsible for the formation of catechin and epicatechin, which are subunits of procyanidins, the main class of polyphenols in the açaí seeds.These proteins showed the same pattern of deposition, in which higher abundances were seen in the S1 and S2 stages. The dataset we offer now is a valuable starting point for a wide range of research aimed at exploiting the biotechnological potential of a troublesome by-product of the depulping process of açaí fruits.

2024-07-02 | PXD034218 | Pride

Environmentally Induced Epigenetic Transgenerational Inheritance of Somatic Transcriptomes

Project description:Environmentally induced epigenetic transgenerational inheritance of adult onset disease involves a variety of phenotypic changes suggesting a general alteration in genome activity. Investigation of eleven different tissue transcriptomes in male and female F3 generation vinclozolin versus control lineage rats demonstrated all tissues examined had unique transgenerational transcriptomes. Common cellular pathways and processes were identified among the tissues. A bionetwork analysis identified gene modules with coordinated gene expression and each had unique gene networks regulating tissue specific gene expression and function. A large number of statistically significant over-represented clusters of differentially expressed genes were identified and termed M-bM-^@M-^\Epigenetic Control RegionsM-bM-^@M-^]. Combined observations demonstrate that all tissues derived from the epigenetically altered germ line develop transgenerational transcriptomes unique to the tissue, but common epigenetic control regions in the genome appear to in part coordinately regulate these tissue specific transcriptomes. This systems biology approach provides insight into the molecular mechanisms involved in the epigenetic transgenerational inheritance of a variety of adult onset disease phenotypes. We used microarrays to determine genes expressed differentially in rats 11 male or female smatic tissues -male heart, kidney, liver, testis, prostate, seminal vesicles; female heart, kidney, liver, ovary, uterus - due to Vinclozolin treatments of their grand-grandmothers. For each of 11 male or female smatic tissues, RNA samples from 2 treatment groups - control (Con) and vinclozolin (Vin) - were compared to each other. Each treatment groups contained 3 biological replica. RNA for each replica was pooled from 2 individual animals.

2012-06-30 | E-GEOD-35839 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data