We reported transcriptional characterization of Treg and Tconv cells from thymic, splenic, and visceral adipose tissue (VAT) of vTreg53 TCR transgenic mice and control littermates. We examined the effect of Foxp3 on splenic and VAT CD4+ T cell transcriptome. We profiled gene expression in a novel PPARg+ splenic Treg population. We uncovered that the characteristic phenotype of VAT Treg cells was acquired in two stages. Overall design: Gene expression profiles of thymic, splenic, VAT Treg, Tconv, and Foxp3-transduced Tconv cells from vTreg53 TCR transgenic and PPARg reporter mice.
TCR Transgenic Mice Reveal Stepwise, Multi-site Acquisition of the Distinctive Fat-Treg Phenotype.
Specimen part, Cell line, Subject
View SamplesWe report age-related gene expression of Treg cells isolated from injured muscle and spleen. Male C57BL/6 Foxp3-GFP reporter mice were injured intramuscularly with cardiotoxin. Tregs were sorted directly into Trizol from injured muscle and spleen 4 days post-injury. Overall design: Gene expression profiling of muscle and splenic Tregs from 2- vs >6-month old mice (biological duplicate for each).
Poor Repair of Skeletal Muscle in Aging Mice Reflects a Defect in Local, Interleukin-33-Dependent Accumulation of Regulatory T Cells.
Sex, Age, Subject
View SamplesWe report gene expression of Treg cells isolated from injured muscle in IL-33 vs PBS treated mice. Male Foxp3-GFP C57BL/6 reporter (2 months old) mice were injured intramuscularly with cardiotoxin/rIL-33 (0.3 ug/muscle). Tregs were sorted directly into Trizol from injured muscle 4 days post-injury. Overall design: Gene expression profiling of muscle Tregs from IL-33 vs PBS injured mice.
Poor Repair of Skeletal Muscle in Aging Mice Reflects a Defect in Local, Interleukin-33-Dependent Accumulation of Regulatory T Cells.
Sex, Age, Treatment, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A special population of regulatory T cells potentiates muscle repair.
Sex, Age, Specimen part, Treatment, Time
View SamplesA 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--vis their two spleen counterparts.
A special population of regulatory T cells potentiates muscle repair.
Sex, Age, Specimen part, Treatment, Time
View SamplesA 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.
A special population of regulatory T cells potentiates muscle repair.
Sex, Age, Specimen part, Treatment, Time
View SamplesGlobal 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.
A special population of regulatory T cells potentiates muscle repair.
Age, Specimen part, Treatment, Time
View SamplesCD4+Foxp3+ regulatory T cells (Tregs) accumulate in skeletal muscle from dystrophin-deficient mdx mice. Analysis of global gene expression in muscles from mdx mice treated with anti-CD25 compared with muscles from mdx mice treated with control antibody revealed that Tregs partially protect mdx mice from muscle pathology and promote muscle repair/regeneration.
A special population of regulatory T cells potentiates muscle repair.
Sex, Age, Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The atypical mitogen-activated protein kinase ERK3 is essential for establishment of epithelial architecture.
Specimen part, Treatment
View SamplesEstablishment and maintenance of epithelial architecture are essential for embryonic development and adult physiology. Here, we show that ERK3, a poorly characterized atypical MAPK, regulates epithelial architecture in vertebrates. In Xenopus embryonic epidermal epithelia, ERK3 knockdown impairs adherens and tight junction protein distribution, as well as tight junction barrier function, resulting in epidermal breakdown. Moreover, in human breast epithelial cancer cells, inhibition of ERK3 expression induces thickened epithelia with aberrant adherens and tight junctions. Microarray results suggest an involvement of TFAP2A, a transcription factor important for epithelial gene expression, in ERK3-dependent gene expression changes. TFAP2A knockdown phenocopies ERK3 knockdown in both Xenopus embryos and human cells, and ERK3 is required for full activation of TFAP2A-dependent transcription. Our findings thus reveal that ERK3 regulates epithelial architecture, possibly in cooperation with TFAP2A.
The atypical mitogen-activated protein kinase ERK3 is essential for establishment of epithelial architecture.
Specimen part, Treatment
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