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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

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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

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]

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

2019-11-17 | GSE139664 | GEO

White adipose tissues: amphiregulin overexpression

Project description:Transcriptional profiling of transgenic mice specifically expressing amphiregulin in white adipose tissues. The objective of this study is to explore gene expression profiles of adipose tissues in response to amphiregulin overexpression.

2017-09-15 | GSE103875 | GEO

Regulatory T cells from injured skeletal muscle

Project description:A phenotypically and functionally distinct population of CD4+ Foxp3+ T cells (Tregs) rapidly accumulates in acutely injured skeletal muscle of mice, just as invading myeloid-lineage cells switch from a pro-inflammatory to a pro-regenerative state. Analysis of gene expression of Tregs and CD4+Foxp3- T cells (Tconvs) from injured muscle and spleen revealed that the transcriptome of muscle Treg cells is distinct from that of splenic Tregs. A set of genes is uniquely expressed by muscle Tregs, while another set is over-expressed by the two muscle populations vis-à-vis their two spleen counterparts. 6 wk-old Foxp3-ires-GFP mice were injured in skeletal muscles with cardiotoxin. Four and fourteen days later, Tregs and Tconvs from spleen and muscle were double-sorted into Trizol. To reduce variability, cells from multiple mice were pooled for sorting, and three replicates were generated for all groups. RNA from 1.5-2.5 x 104 cells was amplified, labeled, and hybridized to Affymetrix Mouse Gene 1.0 ST Arrays.

2013-12-15 | E-GEOD-50096 | biostudies-arrayexpress

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