Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of Amphiregulin on global gene expression in injured skeletal muscle in the presence or absence of CD4+Foxp3+ regulatory T cells (Tregs).

ABSTRACT: Global gene expression analysis of injured skeletal muscle showed that amphiregulin (Areg), a growth factor over-expressed by muscle Treg cells, enhances muscle regeneration both in the presence and in the absence of Tregs.

ORGANISM(S): Mus musculus

PROVIDER: GSE50097 | GEO | 2013/12/15

SECONDARY ACCESSION(S): PRJNA216023

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of Amphiregulin on global gene expression in injured skeletal muscle in the presence or absence of CD4+Foxp3+ regulatory T cells (Tregs).

Project description:Global gene expression analysis of injured skeletal muscle showed that amphiregulin (Areg), a growth factor over-expressed by muscle Treg cells, enhances muscle regeneration both in the presence and in the absence of Tregs. Foxp3-DTR+ and Foxp3-DTR- mice were injured with cardiotoxin in TA muscle at day 0 and treated with diphtheria toxin every other day from day 0 until dissection. Amphiregulin or PBS were administered im on day 0 and ip every other day until dissection. TA muscle was flash-frozen and RNA was extracted using Trizol. RNA from whole tissue samples was amplified, labeled, and hybridized to Affymetrix Mouse Gene 1.0 ST Arrays.

2013-12-15 | E-GEOD-50097 | biostudies-arrayexpress

Gene expression profiling of injured skeletal muscle in the presence or absence of CD4+Foxp3+ regulatory T cells (Tregs).

Project description:A comparative analysis of gene expression of injured skeletal muscle from wild-type (Foxp3-DTR-) and Treg-depleted (Foxp3-DTR+) mice showed that Treg cells are critical for effective repair and regeneration of acute injury of skeletal muscle. Foxp3-DTR+ and Foxp3-DTR- mice were injured with cardiotoxin in TA muscle at day 0 and treated with diphtheria toxin every other day from day 0 until dissection on day 4 or 8. TA muscle was flash-frozen and RNA was extracted using Trizol. RNA from whole tissue samples was amplified, labeled, and hybridized to Affymetrix Mouse Gene 1.0 ST Arrays.

2013-12-15 | E-GEOD-50094 | biostudies-arrayexpress

Gene expression profiling of injured skeletal muscle in the presence or absence of CD4+Foxp3+ regulatory T cells (Tregs).

2013-12-15 | GSE50094 | GEO

Amphiregulin mediates non-cell-autonomous effect of senescence on reprogramming

Project description:Cellular senescence is an irreversible growth arrest with a highly dynamic secretome, termed the senescence-associated secretory phenotype (SASP). Senescence has been implicated in somatic reprogramming to pluripotency. The cell-intrinsic proliferation arrest is a barrier for reprogramming, whereas the SASP facilitates the cell fate conversion in nonsenescent cells. However, the mechanisms by which reprogramming-induced senescence regulates cell plasticity are not well understood. Here, we have further investigated how the heterogeneity of paracrine senescence impacts reprogramming. We show that senescence promotes in vitro reprogramming in a stress-dependent manner. We identified a catalog of SASP factors and pathways potentially involved in the cell fate conversion using an unbiased proteomic analysis. Amphiregulin (AREG), a growth factor frequently secreted by the senescent cells, promotes in vitro reprogramming by accelerating proliferation and MET via the EGFR signaling pathway. Of note, AREG treatment diminished the negative effect of donor age on reprogramming. Finally, AREG enhances in vivo reprogramming in the skeletal muscle. Hence, senescence could facilitate cellular plasticity via various SASP factors to promote reprogramming and tissue repair.

2022-07-28 | PXD028590 | Pride

The EGF Receptor Ligand Amphiregulin Controls Cell Division via FoxM1

Project description:We analyzed the effect of tetracycline (Tet)-inducible amphiregulin (AREG) silencing on the transcriptome of immortalized human N/TERT keratinocytes in the presence or absence of exogenous rhEGF. Tetracycline-mediated AREG silencing significantly altered the expression of 2,331 genes, 623 of which were not normalized towards normal by treatment with EGF. Genes irreversibly up-regulated by suppression of AREG overlapped with genes involved in keratinocyte differentiation. A significant proportion of the irreversibly down-regulated genes featured upstream binding sites recognized by FoxM1

2016-06-23 | GSE70230 | GEO

Transcriptomic profile of endogenous Tregs in mouse injured bone, muscle, skin and heart tissues compared to healthy spleen Tregs

Project description:We aimed to identify the changes in gene expression profile of Tregs isolated from the injured bone, muscle, skin and heart, compared to healthy (uninjured) spleen Tregs. The bone injury consisted of calvarial bone defects, the muscle injury involved volumetric muscle loss defect in the quadriceps and the skin injury involved full-thickness punch-biopsy wounds. The heart injury was performed using the left coronary artery ligation to induce myocardial infarction (MI). The Tregs accumulating within the injured tissues were isolated and purified by fluorescence activated cell sorting (FACS), at 7 days post-injury (which is the peak of Treg accumulation within these tissues post-injury).

2024-05-31 | GSE228871 | GEO

HDAC3 maintains oocyte meiosis arrest by repressing amphiregulin expression before the LH surge [HDAC3cKO]

Project description:It is known that granulosa cells (GCs) mediate gonadotropin-induced oocyte meiosis resumption by releasing EGF-like factors in mammal, however, the detail molecular mechanisms remain unclear. Here, we demonstrate that luteinizing hormone (LH) surge induced histone deacetylase 3 (HDAC3) downregulation in GCs is essential for oocyte maturation. Before the LH surge, HDAC3 is highly expressed in GCs. Transcription factors, such as FOXO1, mediates recruitment of HDAC3 to the amphiregulin (Areg) promoter, which suppresses AREG expression. With the LH surge, decreased HDAC3 in GCs enables histone H3K14 acetylation and binding of the SP1 transcription factor to the Areg promoter to initiate AREG transcription and oocyte maturation. Conditional knockout of Hdac3 in granulosa cells in vivo or inhibition of HDAC3 activity in vitro promotes the maturation of oocytes independent of LH. Taking together, HDAC3 in GCs within ovarian follicles acts as a negative regulator of EGF-like growth factor expression before the LH surge.

2019-11-17 | GSE139663 | GEO

HDAC3 maintains oocyte meiosis arrest by repressing amphiregulin expression before the LH surge [oocyte-transcriptome]

2019-11-17 | GSE139665 | GEO

HDAC3 maintains oocyte meiosis arrest by repressing amphiregulin expression before the LH surge [mGC-HDACi]

2019-11-17 | GSE139664 | GEO

Pharmacological impacts of Mucopolysacccharide Polyphosphates in skin involves inhibition of Amphiregulin-mediated signals in keratinocytes

Project description:The epidermis, the most superficial layer of human skin, serves a critical barrier function, protecting the body from external pathogens and allergens. Dysregulation in the epidermal differentiation process contributes to barrier dysfunction and is implicated in the pathology of various dermatological diseases, including atopic dermatitis (AD). Mucopolysaccharide polysulfate (MPS) is used as a moisturizing agent for xerosis in AD patients. However, its mechanism of action on keratinocytes, the main constituent of the epidermis, remains unclear. In this study, we investigated the impact of MPS on keratinocytes by subjecting adult human epidermal keratinocyte (HEKa) cells and three-dimensional cultured keratinocytes to MPS treatment, followed by transcriptome analysis. The analysis revealed that MPS treatment enhances keratinocyte differentiation and suppresses proliferation. We focused on amphiregulin (AREG), a membrane protein that belongs to the epidermal growth factor (EGF) family and possesses a heparin-binding domain, as a significant target of the MPS among the genes altered by MPS. It is revealed that MPS exerts an inhibitory effect directly on AREG, rather than on the EGF receptor or other members of the EGF family. Furthermore, it is suggested that AREG leads to a reduction in epidermal barrier function, whereas MPS contributes to barrier enhancement through AREG inhibition. Collectively, these findings suggest that MPS modulates barrier function through the inhibition of AREG, offering insights into potential therapeutic strategies for skin barrier restoration.

2024-07-03 | GSE268656 | GEO

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