Role of IL33 on muscle regneration in aging
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE76695 | GEO | 2016/01/10
SECONDARY ACCESSION(S): PRJNA308349
REPOSITORIES: GEO
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Project description:We compare the effect of IL-33 vs PBS on muscle regneration from 22-month old mice 8 days post-injury. These analyses from whole muscle provide insight into the role of IL-33 on regeneration in the context of aging. The tibialis anterior muscle from male C57BL/6 mice (22 months old) were cryo-injured using a liquid nitrogen chilled metal probe for 8 seconds. Mice received 2 ug of rIL-33 via intraparitoneal injection the day prior and the day following cryoinjury. 8 days post-injury whole muscle was harvested and snap frozen in liquid nitrogen. Whole muscle was then homogenized directly in TriZol and gene expression profiling was performed on Affymetrix Mouse Gene 1.0 ST Arrays.
2016-01-10 | E-GEOD-76695 | biostudies-arrayexpress
Project description:We 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. Gene expression profiling of muscle Tregs from IL-33 vs PBS injured mice.
2016-01-12 | E-GEOD-76722 | biostudies-arrayexpress
Project description:We 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.
2016-01-12 | GSE76722 | GEO
Project description:Mitochondrial fusion and fission proteins regulate mitochondrial quality control and mitochondrial metabolism. In turn, mitochondrial dysfunction is associated with aging, although its causes are still under debate. Here, we show that aging is characterized by a progressive reduction of Mitofusin 2 (Mfn2) in mouse skeletal muscle and that skeletal muscle Mfn2 ablation in mice generates a gene signature linked to aging. Furthermore, muscle Mfn2-deficient mice show unhealthy aging characterized by altered metabolic homeostasis and sarcopenia. Mfn2 deficiency impairs mitochondrial quality control, which contributes to an exacerbated age-related mitochondrial dysfunction. Surprisingly, aging-induced Mfn2 deficiency triggers a ROS-dependent retrograde signaling pathway through induction of HIF1 transcription factor and BNIP3. This pathway ameliorates mitochondrial autophagy and minimizes mitochondrial damage. Our findings reveal that repression of Mfn2 in skeletal muscle during aging is determinant for the loss of mitochondrial quality, contributing to age-associated metabolic alterations and loss of muscle fitness. Quadriceps muscle from four mice per genotype were used (Control young (6 month-old), Mfn2KO young (6-month-old), control old (22-month-old) and Mfn2KO old (22-month-old)
2016-08-08 | E-GEOD-71501 | biostudies-arrayexpress
Project description:Dusp5 regulates ERK phosporylation following IL-33 receptor ligation in cultured eosinophils. Dusp5 deficient eosinophils show increased ERK phosphorylation, and as a result are less apoptotic. Since ERK stimulation results in downstream activation of transcription factors, we are utilizing a microarray approach to find alterations in gene expression to uncover potential mechanisms for increased cell survival. Day 12 bone marrow derived eosinophils from Dusp5+/+ and Dusp5-/- mice (5 mice per genotype) were left untreated (media only) or IL-33 (25ng/ml) stimulated for 4 hours. Treated cells were washed with ice cold PBS and cell pellets were directly lysed in RLT buffer (Qiagen) followed by immediate RNA isolation (RNEasy plus mini kit with genomic DNA eliminator columns). Sample group names: Group 1- Dusp5+/+ Untreated (N=5) Group 2- Dusp5-/- Untreated (N=5) Group 3- Dusp5+/+ IL-33 4hrs (N=5) Group 4- Dusp5-/- IL-33 4hrs (N=5) Sample Names: Group 1- BM Eos unstimulated WT-1....WT-5 Group 2- BM Eos unstimulated Dusp5-/- -1......Dusp5-/- -5 Group 3- BM Eos IL-33 4hrs WT-1....WT-5 Group 4- BM Eos IL-33 4hrs Dusp5-/- -1......Dusp5-/- -5
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Project description:We analyzed the total proteome of group 2 innate lymphoid cells (ILC2s) after different stimulation with interleukin-33 (IL-33), a cytokine playing a critical role in human asthma, and TL1A, a TNF-family cytokine also known to activate ILC2s. Upon combined stimulation with IL-33 plus TL1A, we show that lung ILC2s produce high amounts of IL-9 and acquire a transient ‘ILC9’ phenotype. This phenotype is characterized by simultaneous production of large amounts of type 2 cytokines (IL-5, IL-13 and IL-9), induction of the IL-2 receptor CD25 (Il2ra), and of the transcription factors IRF4, JunB and BATF, that form immune-specific complexes known to induce IL-9 expression.
2024-03-05 | PXD041987 | Pride
Project description:A distinct population of Foxp3+CD4+ regulatory T (Treg) cells promotes repair of acutely or chronically injured skeletal muscle. The accumulation of these cells depends critically on interleukin (IL)-33 produced by local mesenchymal stromal cells (mSCs). An intriguing physical association between muscle nerves, IL-33+ mSCs and Tregs has been reported, and begs a deeper exploration of this cell triumvirate. Here we evidence a striking proximity between IL-33+ muscle mSCs and both large-fiber nerve bundles and small-fiber sensory neurons; report that muscle mSCs transcribe an array of genes encoding neuropeptides, neuropeptide receptors and other nerve-related proteins; define muscle mSC subtypes that express both IL-33 and the receptor for the calcitonin-gene-related peptide (CGRP); and demonstrate that up- or down- tuning of CGRP signals augments or diminishes, respectively, IL-33 production by muscle mSCs and later accumulation of muscle Tregs. Indeed, a single injection of CGRP induced much of the genetic program elicited in mSCs early after acute skeletal muscle injury. These findings highlight neural/stromal/immune-cell cross-talk in tissue repair, suggesting future therapeutic approaches.
2020-02-10 | GSE143424 | GEO
Project description:A distinct population of Foxp3+CD4+ regulatory T (Treg) cells promotes repair of acutely or chronically injured skeletal muscle. The accumulation of these cells depends critically on interleukin (IL)-33 produced by local mesenchymal stromal cells (mSCs). An intriguing physical association between muscle nerves, IL-33+ mSCs and Tregs has been reported, and begs a deeper exploration of this cell triumvirate. Here we evidence a striking proximity between IL-33+ muscle mSCs and both large-fiber nerve bundles and small-fiber sensory neurons; report that muscle mSCs transcribe an array of genes encoding neuropeptides, neuropeptide receptors and other nerve-related proteins; define muscle mSC subtypes that express both IL-33 and the receptor for the calcitonin-gene-related peptide (CGRP); and demonstrate that up- or down- tuning of CGRP signals augments or diminishes, respectively, IL-33 production by muscle mSCs and later accumulation of muscle Tregs. Indeed, a single injection of CGRP induced much of the genetic program elicited in mSCs early after acute skeletal muscle injury. These findings highlight neural/stromal/immune-cell cross-talk in tissue repair, suggesting future therapeutic approaches.
2020-02-10 | GSE143425 | GEO
Project description:A distinct population of Foxp3+CD4+ regulatory T (Treg) cells promotes repair of acutely or chronically injured skeletal muscle. The accumulation of these cells depends critically on interleukin (IL)-33 produced by local mesenchymal stromal cells (mSCs). An intriguing physical association between muscle nerves, IL-33+ mSCs and Tregs has been reported, and begs a deeper exploration of this cell triumvirate. Here we evidence a striking proximity between IL-33+ muscle mSCs and both large-fiber nerve bundles and small-fiber sensory neurons; report that muscle mSCs transcribe an array of genes encoding neuropeptides, neuropeptide receptors and other nerve-related proteins; define muscle mSC subtypes that express both IL-33 and the receptor for the calcitonin-gene-related peptide (CGRP); and demonstrate that up- or down- tuning of CGRP signals augments or diminishes, respectively, IL-33 production by muscle mSCs and later accumulation of muscle Tregs. Indeed, a single injection of CGRP induced much of the genetic program elicited in mSCs early after acute skeletal muscle injury. These findings highlight neural/stromal/immune-cell cross-talk in tissue repair, suggesting future therapeutic approaches.
2020-02-10 | GSE143426 | GEO
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2023-06-12 | GSE180225 | GEO