Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Interleukin-33 in experimental kidney fibrosis

ABSTRACT: Interleukin-33 in experimental kidney fibrosis

PROVIDER: PRJNA630481 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Interleukin-33 in experimental kidney fibrosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-05-06 | GSE149918 | GEO

Knockdown of interleukin-33 in human fibroblasts

Project description:Interleukin (IL)-33 is a cytokine that appears to mediate fibrosis by signaling via its receptor ST2 (IL-33R/IL1RL1). It is also, however, a protein that after synthesis is sorted to the cell nucleus, where it appears to affect chromatin folding. Here we describe a novel role for nuclear IL-33 in regulating the fibroblast phenotype in murine kidney fibrosis driven by unilateral ureteral obstruction. Transcriptional profiling of IL-33-deficient kidneys 24h after ligation revealed enhanced expression of fibrogenic genes and enrichment of gene sets involved in extracellular matrix formation and remodeling. These changes relied on intracellular effects of IL-33, because they were not reproduced by treatment with a neutralizing antibody to IL-33 that prevents IL-33R/ST2L receptor signaling nor were they observed in IL33R/ST2-deficient kidneys. To further explore the intracellular function of IL-33, we established transcription profiles of human fibroblasts, observing that knockdown of IL-33 skewed the transcription profile from an inflammatory towards a myofibroblast phenotype, reflected in higher levels of COL3A1, COL5A1 and transgelin protein, as well as lower expression levels of IL6, CXCL8, CLL7 and CCL8. In conclusion, our findings suggest that nuclear IL-33 in fibroblasts dampens the initial profibrotic response until persistent stimuli, as enforced by UUO, can override this protective mechanism.

2020-05-06 | GSE149917 | GEO

Glioma cells response Interleukin-33 (IL-33) [microarray]

Project description:Glioma cells response Interleukin-33 (IL-33) [microarray]

| PRJNA642838 | ENA

Mouse immune cells response Interleukin-33 (IL-33) [nanostring]

Project description:Mouse immune cells response Interleukin-33 (IL-33) [nanostring]

| PRJNA642836 | ENA

A proteomic landscape of the spatiotemporal influence of Interleukin-33 (IL-33) in monocytes

Project description:Interleukin-33 (IL-33), a member of the IL-1 superfamily cytokines, is an endogenous danger signal and a nuclear-associated cytokine. It is one of the essential mediators of both innate and adaptive immune responses. Aberrant IL-33 signaling has been demonstrated to play a defensive role against various infectious and inflammatory diseases. Although the signaling responses mediated by IL-33 have been previously reported, the temporal signalingdynamicsare yet to be explored. Towards this end,we applied quantitative temporal phosphoproteomics analysis to elucidate pathways and proteins induced by IL-33 in THP1 monocytes. Employing TMT labeling-based quantitation and titanium dioxide (TiO2)-based phosphopeptide enrichment strategy followed by mass spectrometry analysis, we identified 14,515 phosphorylation sites mapping to 4,174 proteins across (0 min to 240 mins)time points.

2022-02-16 | PXD028673 | Pride

Dataset of spatiotemporal influences of interleukin IL-1 family cytokine: Interleukin-33 on cellular signal transduction pathways

Project description:Interleukin-33 (IL-33) is a member of the IL-1 family of cytokines that play a central role in the regulation of immune responses. IL-33 signaling, from the early signaling events triggered by the ligand-activated receptor to result in activation of early and late signaling events, such as proteome changes. In this study, THP1 (monocyte) cell line model was stimulated with IL-33 (50 ng/ml) for varying duration (5, 10, 15, 30, 40, 60, 120 and 240 mins). We carried out in-depth proteomic analysis using high-resolution LC-MS/MS. Our analysis resulted in the identification of 64,030 peptides corresponding to 7947 protein groups. Differentially regulated proteins identified in this study could be targeted for developing an inflammatory immune response.

2022-02-17 | PXD024385 | Pride

Knockdown of interleukin-33 in human fibroblasts

Project description:Knockdown of interleukin-33 in human fibroblasts

| PRJNA630484 | ENA

Kidney VISTA prevents IFNγ-IL-9 axis-mediated tubulointerstitial fibrosis after acute glomerular injury

Project description:Backgrounds: The present study addressed whether V-domain Ig suppressor of T cell activation (VISTA), constitutively expressed in kidney macrophages, has a protective role in tubulointerstitial fibrotic transformation after acute antibody-mediated glomerulonephritis. Methods: Wild-type (WT) and VISTA-deficient (Vsir-/-, KO) mice were treated with nephrotoxic serum to induced acute antibody-mediated glomerulonephritis, and their cytokine and fibrosis profiles were compared. Results: VISTA was highly expressed in kidney macrophages (resident more than infiltrating subset). If VISTA was depleted, tubules suffered further damage after glomerular injury. In damaged Vsir–/– mice, the contact frequency of macrophages with infiltrated T cells increased, and then the immunometabolic characteristics of T cells changed to overproduction of interferon-γ. The Vsir–/– parenchymal tissue cells responded to this altered milieu as more producing interleukin-9, which augmented tubulointerstitial fibrosis and irreversible kidney dysfunction. The blocking antibodies against interferon-γ and interleukin-9 protected above pathological process by VISTA depletion. Conclusions: VISTA is a sentinel protein of kidney macrophages, which prevents tubulointerstitial fibrosis via interferon-γ-interleukin-9 axis after acute antibody-mediated glomerular injury.

2021-08-04 | GSE181163 | GEO

Renal fibrosis mRNA classifier: validation in experimental lithium-induced interstitial fibrosis in the rat kidney

Project description:Metzincins and related genes (MARGS) play important roles in ECM remodeling in fibrotic conditions. In this investigation, gene expression was examined in a rat model to investigate whether the previously described MARGS based fibrosis classifier had diagnostic value in an experimental rat model of lithium-induced renal fibrosis

2017-02-08 | GSE83610 | GEO

Cerebral immune cells in the Interleukin-33 (IL-33) driven tumor microenvironment

Project description:Cerebral immune cells in the Interleukin-33 (IL-33) driven tumor microenvironment

| PRJNA642831 | ENA