Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling

ABSTRACT: To investigate skin aging is an important driver of experimental osteoarthritis(OA) progression in mice via enhanced IL-36 receptor (IL-36R) signaling. we generated epidermis keratinocyte conditional knockout mice (IL-36Ra-cKO) with topical administration of capsid-mutant Adeno-associated virus 2 (AAV2) vector23 encoding Cre recombinase (AAV2-Cre) to IL-36Rafl/fl mice. Subsequently, epidermal skin tissues were collected from IL-36Rafl/fl and IL-36Ra-cKO mice for RNA sequencing analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE263907 | GEO | 2024/05/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

IL-36 signaling in keratinocytes controls early IL-23 production in Aldara®-induced skin inflammation in mice

Project description:IL-36R signaling plays an important role in the pathogenesis of psoriasis. We ought to assess the specific function of IL-36R in keratinocytes for the pathology of Aldara®-induced psoriasis-like skin inflammation. Il36r-/- (KO) and Il36rΔK (DK) mice as well as their littermate controls, respectively Il36r+/+ (WT) and Il36rfl/fl (FL) mice, were challenged with the topical application of Aldara® on one ear during 3 or 7 days. RNASeq was performed on treated (AL) and untreated (CT) ears. Fold change analysis combined with RPKM and RT-qPCR allowed us to identify genes which were specifically regulated by IL-36R signaling in keratinocytes during the course of the treatment. We notably demonstrated that both IL-23 subunits (Il23a and Il12b) fell into this category.

2020-04-23 | GSE143688 | GEO

Proteomic analysis of adult CNS from Rhoa cKOs and CTRs mice

Project description:Oligodendrocyte differentiation and subsequent myelination rely on strict regulatory mechanisms and molecules. Here we aimed at understanding the role of the Rho GTPase RhoA during oligodendrocyte differentiation and myelination in vivo. Using a conditional cell-specific ablation of Rhoa (Rhoa fl/fl mice crossed with Cnp-Cre mice) in oligodendrocytes, we show that RhoA controls the timing and progression differentiation and myelination. To identify putative mechanisms underlying the Rhoa cKO phenotype, we performed quantitative label-free LC-MS/MS proteomics on optic nerves from Rhoa cKO (Rhoa fl/fl Cre+) and control mice (Rhoa fl/fl Cre-) at 30 days post-birth (P30). Manual annotation of the differentially abundant proteins showed a large modulation of several proteins clusters associated with actin cytoskeleton, signal transduction and mitochondria.

2024-11-05 | PXD055052 | Pride

Retinoic Acid Related Receptor Orphan Receptor a (RORa) expressing T regulatory cells thwart type-2 cutaneous allergic inflammation

Project description:We used RNA-sequencing to profile gene expression differences between Tregs from skin and LNs of Foxp3 cre-efyp WT mice. We further compared skin Tregs from control and Foxp3 cre Rora fl/fl (Rora cKO) mice in the steady state and after allergic inflammation was induced using MC903.

2018-03-26 | GSE99086 | GEO

Enhanced IL-36R signaling promotes barrier impairment and inflammation in skin and intestine

Project description:Deficiency in IL-36R antagonist caused by loss of function mutations in IL-36RN leads to DITRA (1), a rare inflammatory human disease that belongs to a subgroup of Generalized Pustular Psoriasis (GPP). Herein, we report a novel functional genetic mouse model of DITRA with enhanced IL-36R signaling analogous to one observed in DITRA patients which supports and provides new insight in our understanding of IL-36 family of molecules in regulating barrier integrity across multiple tissues. Humanized DITRA-like mice displayed increased skin inflammation in preclinical model of psoriasis, and in vivo blockade of IL-36R pathway using anti-human IL-36R antibody ameliorated IMQ-induced skin pathology at both prophylactic and therapeutic treatments. Deeper characterization of the humanized DITRA-like mice revealed that deregulated IL-36R signaling promoted tissue pathology during intestinal injury and led to impairment in mucosal restoration in the repair phase of chronic DSS-induced colitis. Blockade of IL-36R pathway significantly ameliorated DSS-induced intestinal inflammation and rescued the inability of DITRA-like mice to recover from mucosal damage in vivo. Thus, our results indicate a central role for IL-36 in regulating the pro-inflammatory responses in the skin and epithelial barrier function in the intestine suggesting a new therapeutic potential for IL-36R axis in psoriasis and at the later stages of intestinal pathology.

2020-12-18 | GSE161406 | GEO

Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling

Project description:To investigate skin aging is an important driver of experimental osteoarthritis(OA) progression in mice via enhanced IL-36 receptor (IL-36R) signaling. The supernatants from the co-culture of UV-aged mouse primary keratinocytes with synovial fibroblasts were collected to induce mouse primary articular chondrocytes (CCs) to become aging SNL CCs. On this basis, Spesolimab (100ng/ml) was added to culture aging SNL CCs to study the drug's effect on OA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 groups: control CCs, aging SNL CCs, aging SNL CCs+Spesolimab.

2024-05-01 | GSE264103 | GEO

Gene expression in mouse liver depleted of HDAC3

Project description:Liver-specific depletion of HDAC3 leads to liver steatosis (fatty liver), suggesting disregulation of lipid metabolism. This is correlated with changes in lipid metabolic gene expression. Livers depleted of HDAC3 were removed from 12 week old male HDAC3 fl/fl mice (loxP sites flanking exon 4 to 7 of the HDAC3 gene encoding the catalytic domain of HDAC3) one week after the injection of AAV2/8-Tbg-Cre virus. Livers from the HDAC3 fl/fl mice injected with AAV2/8-Tbg-GFP were used as normal controls.

2011-03-11 | GSE25937 | GEO

Decoupling astrocytes in adult mice impairs synaptic plasticity and spatial learning

Project description:To study the role of the gap junction coupled astrocytic network, we generated inducible double knockouts to selectively delete Cx30 and Cx43 from astrocytes in adult mice. Mice carrying loxP-flanked Gjb6 (Cx30fl/fl mice) (Boulay et al., 2013) and Gja1 (Cx43fl/fl mice) (Theis et al., 2003) alleles were crossbred with mice expressing the tamoxifen-sensitive Cre-recombinase CreERT2 under the endogenous GLAST(Slc1a3)-promoter (Mori et al., 2006). Adult, 8-10 week old mice (Cx30fl/fl:Cx43fl/fl:GLASTCreERT2/+, termed cKO) and littermate control mice (Cx30fl/fl:Cx43fl/fl:GLAST+/+) were injected with tamoxifen for 5 consecutive days and hippocampi were isolated for subsequent TMT-based proteomics analysis 90 days after tamoxifen treatment, to study the consequences of astrocyte decoupling and connexin deletion.

2022-03-14 | PXD031136 | Pride

Heterozygous and Homozygous Knock-Out of USP7 mouse models [mouse_RNA-seq]

Project description:RNAseq analysis of USP7 conditional knock-out (cKO) mice. They were designed to flox exon 6 of USP7 and to allow deletion of exon 6 upon expression of Cre recombinase 27. USP7FL/FL mice were bred with Vav1-Cre mice to obtain USP7FL/wt-Vav1-Cre mice (heterozygote). USP7FL/FL-Vav1-Cre mice (homozygote) were obtained via breeding of heterozygous cKO mice.

2021-03-09 | GSE148521 | GEO

Gene expression in mouse liver depleted of HDAC3

2011-03-11 | E-GEOD-25937 | biostudies-arrayexpress

DDX5-sIL-36R in keratinocytes controls skin inflammation

Project description:The DEAD-box (DDX) proteins function in diverse cellular processes including RNA alternative splicing, and are linked to immune-mediated diseases. However, little is known about the roles of DDXs in skin inflammatory diseases. Here, we show that DDX5, one of the founding members of the DDX RNA helicase family, controls skin inflammation and participates in the pathogenesis of psoriasis via regulating IL-36R pre-mRNA splicing. We found that both mRNA and protein of DDX5 are decreased in lesional skin from patients with psoriasis and psoriasis-like mice, and that mice with keratinocyte-specific ablation of DDX5 spontaneously develop psoriasis-like phenotypes. Mechanistically, DDX5 complexes with serine/arginine-rich splicing factor 1(SRSF1) to typically regulate IL-36R pre-mRNA splicing in keratinocytes, which generates mRNAs encoding full-length IL-36R and a previously unknown soluble form of IL-36R (sIL-36R). sIL-36R controls IL-36/IL-36R signaling by competing with IL-36R for IL-36γ ligation. The reduction or deficiency of DDX5 leads to IL-36R pre-mRNA splicing preferring to the generation of IL-36R but not sIL-36R, thereby selectively amplifying inflammatory responses of keratinocytes to IL-36γ and then aggravating cutaneous inflammation in psoriasis. Genetic restoration or intradermal administration of sIL-36R in psoriasis-like mice suppresses IL-36R signaling and alleviates the disease phenotype of psoriasis. Altogether, these data reveal a pathogenic role of DDX5 during psoriasis, and provide mechanistic insights into the regulation of IL-36R splicing and its impact on psoriasis development.

2020-09-09 | PXD021379 |

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