Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from mouse thymus

ABSTRACT: Previous studies have shown that extensive transciptional changes occur in the thymus as the tissue atrophies during aging, and that atrophy is delayed in catalase transgenic (mCat Tg, tg) mice. These studies address whether the transciptional profile of medullary thymic tissue in aged mCat Tg mice retains characteristics of the young medullary tissue or not. We used microarrays to detail transciptional profiles in aged mCat Tg mouse thymus to compare to gene expression in aged wild type mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE189279 | GEO | 2022/02/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Global gene expression in mouse thymic tissue or lymphocytes from young or aged mice, and during induced regeneration

Project description:The thymus begins to atrophy early in life, but maintains the capacity for transient robust re-growth in response to chemical or physical androgen ablation in males. In mice, at age 5 weeks the thymus remains near peak size, while by 12 months it has atrophied by . In response to castration the thymus re-grows to approximately it's peak size after about 20 days when it begins to rapidly re-atrophy. This study contains gene expression data from affymetrix microarrays covering thymic cortical and medullary laser capture microdissected tissue as well as FACS sorted cortical and medullary lymphocytes in young and aged mice, as well as timecourse data during castration induced regrowth.

2019-06-04 | GSE132136 | GEO

MITOCHONDRIAL ANTIOXIDANTS ABATE SARS-COV-2 LETHALITY IN MICE

Project description:SARS-CoV-2 infection inhibits mitochondrial oxidative phosphorylation (OXPHOS), elevates mitochondrial reactive oxygen species (mROS) which activates HIF-1α shifting metabolism toward glycolysis, and causes release of mtDNA which activates the innate immune system. To determine if mitochondrially targeted antioxidants could mitigate these viral effects, we combined in mice hACE2 with mitochondrially-targeted-catalase (mCAT) and showed that SARS-CoV-2 infected hACE2-mCAT mice had decreased weight loss; decreased circulating levels of mtDNA, IL-1β, and INF-β; and decreased lung HIF-1α and nucleocapsid protein levels. RNA-sequencing of infected lungs revealed that mCAT upregulated OXPHOS gene expression and downregulated glycolytic, innate immune, and HIF-1α-target gene expression. The mitochondrial antioxidant drug EUK8 had the same effect as mCAT potentially providing a pharmacological therapy for COVID-19 which is not subject to viral mutational resistance.

2024-07-31 | GSE246312 | GEO

Transgenic overexpression of Pla2g10

Project description:Microarray gene profiling of thymus from PLA2G10-Tg mice in comparison with that from control mice. Pla2g10-Tg/+ mice and littermate controls (C57BL/6 background); 6-months old; thymus; pooled from 4 mice for each genotype.

2016-01-29 | E-GEOD-77336 | biostudies-arrayexpress

Expression data from adult mouse brain astrocytes

Project description:We aimed to investigate whether reduction of mitochondrial reactive oxygen species (mROS) in adult astrocytes altered the transcriptional profile in vivo. To do so, we used a genetic approach expressing a version of the catalase enzyme within the mitochondria of astrocytes. Astrocytes were acutely isolated from the brains of adult GFAP-mCAT and control mice by the immunomagnetic approach and subjected to a whole-genome transcriptomics array analysis. We used microarrays to detail the whole genome changes modulated by mROS levels in astrocytes.

2019-02-04 | GSE124130 | GEO

Overexpression of catalase delays age-related cardiac disease by preventing oxidative cysteine modifications

Project description:Reactive protein cysteine thiolates are instrumental in redox regulation. Aging associated to oxidative stress, can impair redox signaling by damaging essential cysteine thiolates. Our initial study found that cardiac-specific overexpression of catalase, can protect from oxidative stress and delay cardiac aging in mice. The Project aimed to investigate differential reversible cysteine thiol oxidation in cardiac proteome of wild type and Cat transgenic (Tg) mice, using “Tandem Mass Tag” (TMT) labeling strategy and mass spectrometry. Our results show globally decreased cysteine thiol occupancy in cardiac proteins in Cat Tg mice. The majority of proteins with differentially modified thiols may be involved in pathways of aging and cardiac disease including cellular stress response, proteostasis and apoptosis. Overexpressed catalase may modulate these protein cysteine thiol oxidations resulting in delayed cardiac aging and related pathologies.

2018-10-24 | PXD002479 | Pride

mRNA expression profile of medullary thymic epithelial cells - mTECs - from pre-diabetic NOD mice

Project description:The oligo microarrays were used to determine mRNA expression profiles of medullary thymic epithelial cells (mTECs) isolated from thymus of pre-diabetic NOD mice.

2012-08-11 | E-MEXP-3358 | biostudies-arrayexpress

Transgenic overexpression of Pla2g10

Project description:Microarray gene profiling of thymus from PLA2G10-Tg mice in comparison with that from control mice.

2016-01-29 | GSE77336 | GEO

microRNA expression profile from medullary thymic epithelial cells - mTECs - from pre-diabetic NOD mice

Project description:Due to high sequence identity between human and M. musculus microRNAs, we used in this study human microRNA microarrays to determine microRNA expression profiles of medullary thymic epithelial cells (mTECs) from thymus of pre-diabetic NOD mice.

2012-08-11 | E-MEXP-3357 | biostudies-arrayexpress

Mitochondrial-derived Oxidative Stress Alters Gene Expression and DNA Methylation in the Heart [expression]

Project description:Mitochondrial dysfunction causes oxidative stress and cardiomyopathy. Oxidative stress also is a side effect of dideoxynucleoside antiretrovirals (NRTI) and NRTI-induced cardiomyopathy. We show here that treatment with the NRTI AZT (1-[(2R,4S,5S)-4-azido-5-(hydroxymethyl)oxolan-2-yl]-5-methylpyrimidine-2,4-dione) modulates cardiac gene expression epigenetically through production of mitochondrially-derived reactive oxygen species (ROS). Transgenic mice with ubitquitous expression of mitochondrially-targeted catalase (MCAT) and C57BL/6 wild-type mice littermates (WT) were administered AZT (p.o., 0.22 mg/d; 35 days), and cardiac DNA and mRNA were isolated. In AZT-treated WT, 95 cardiac genes were differentially expressed compared to vehicle-treated WTs. When MCAT mice were treated with AZT, each of those 95 genes reverted to the pattern of vehicle-treated WTs. In AZT-treated WT hearts, Mthfr (5,10-methylenetetrahydrofolate reductase; a critical enzyme in synthesis of methionine cycle intermediates including S-adenosylmethionine (SAM)), was overexpressed. AZT caused hypermethylation (47%) and hypomethylation (53%) of differentially methylated DNA regions in WT cardiac DNA. AZT-treated MCAT heart DNA exhibited greater hypermethylation (91%) and less hypomethylation (9%) compared to vehicle-treated controls. Results show that mitochondrially-derived oxidative stress in the heart that is caused by AZT hinders cardiac DNA methylation, alters cardiac gene expression, and promotes characteristic pathophysiological changes of cardiomyopathy. This mechanism for NRTI toxicity offers insight into long-term side effects from these commonly used antiviral agents.

2016-05-23 | GSE54893 | GEO