Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inhibition of interleukin-1 receptor-associated kinase (IRAK)-4 provides partial rescue of interleukin-1 beta induced functional and gene expression changes in equine tendon cells.

ABSTRACT: We investigated if the daily application of the interleukin-1 receptor-associated kinase (IRAK)-4 inhibitor PF-06650833 could rescue the effect of interleukin-1 beta on equine tendon cells cultured in 3D

ORGANISM(S): Equus caballus

PROVIDER: GSE300167 | GEO | 2025/11/06

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Inhibition of interleukin-1 receptor-associated kinase (IRAK)-4 provides partial rescue of interleukin-1 beta induced functional and gene expression changes in equine tendon cells.

Project description:Inhibition of interleukin-1 receptor-associated kinase (IRAK)-4 provides partial rescue of interleukin-1 beta induced functional and gene expression changes in equine tendon cells.

| PRJNA1279161 | ENA

Interleukin-1b in Tendon Injury Enhances Reparative Gene and Protein Expression in Mesenchymal Stem Cells

Project description:Intralesional mesenchymal stem cell (MSC) therapy has improved tissue architecture and reinjury rates in equine tendon injury; however, the mechanisms by which they promote repair are still being investigated. Therefore, the objectives of this study were to determine how the predominate pro-inflammatory cytokines present in a surgically induced model of equine tendon injury modulate MSC gene and protein expression.

2022-07-26 | GSE208569 | GEO

Equine energy-storing SDFT tendon development, Proteomic analysis of IFM and fascicles through development

Project description:Equine energy-storing SDFT tendon development, Proteomic analysis of IFM and fascicles through development

2021-09-08 | PXD012169 | Pride

Equine tendon LC-MSMS, C4PR_LIV

Project description:the aim of this study was to isolate, characterise and compare the proteome of the IFM and fascicular matrix (FM) in the equine superficial digital flexor tendon (SDFT). We hypothesised that the proteomic profile would differ between the FM and the IFM, with greater complexity and faster turnover in the IFM. Regions of the SDFT were isolated using laser capture microdissection and the protein profile assessed using mass spectrometry. 246 proteins were identified in the IFM, and 141 were identified in the FM. 60 proteins showed a 2-fold difference in abundance between the IFM and FM, including greater abundance of collagen-III and cellular proteins in the IFM, and higher levels of collagens-I and XII, and fibromodulin in the FM. A greater number of neopeptides were identified in the IFM, indicating more rapid turnover than in the FM. There were few alterations in protein abundance with ageing, but the number of neopeptides decreased with age in the IFM specifically, suggesting a decrease in IFM turnover in aged individuals. These results support the hypothesis, showing distinct protein profiles and indicating more rapid turnover in the IFM than in the FM, which appears to decline with ageing in the IFM specifically. This may result in alterations in IFM mechanical properties in aged tendon, contributing to age-related tendon injury.

2016-02-08 | PXD002979 | Pride

Expression data from MALP-2-stimulated macrophages from wild-type, IRAK-2-/- and IRAK-1-/IRAK-2-/- mice

2008-03-08 | GSE10765 | GEO

Transcription profiling of mouse MALP-2-stimulated macrophages FROM wild-TYPE, IRAK-2-/- AND IRAK-1-/IRAK-2-/- animals

Project description:IL-1R-associated kinases (IRAKs) participate in Toll-like receptor (TLR) signal transduction. MALP-2 is a TLR2 ligand, and stimulation of macrophages with MALP-2 activates expression of various genes including proinflammatory cytokines. We used microarrays to examine influence of IRAK-2 or IRAK-1/IRAK-2 deficiency in MALP-2-inducible gene expression. Experiment Overall Design: Peritoneal macrophages from wild-type, IRAK-2-/- and IRAK-1/IRAK-2 mice were stimulated with MALP-2 for 0, 2, 4, and 8 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.

2008-04-05 | E-GEOD-10765 | biostudies-arrayexpress

Exogenous interleukin-1 beta stimulation regulates equine tenocyte function and gene expression which can only be rescued by pharmacological inhibition of interleukin 1 receptor, but not nuclear factor kappa B, signalling

Project description:We investigated how Interleukin 1 beta impacts equine tenocyte function and global gene expression in 3D culture and determined if these effects could be rescued by pharmacologically inhibiting nuclear factor-κB or interleukin 1 signalling.

2023-06-14 | GSE221370 | GEO

Partial Tendon Injury at the Tendon-to-Bone Enthesis Activates Skeletal Stem Cells

Project description:Partial tendon-to-bone interface (TBI) injuries heal in a mechanically inferior manner and redevelop healthy uninjured tissue morphology. The origin of the cells involved in tendon-to-bone healing remains unknown. We employed a rigorous approach to evaluate if mouse skeletal stem cells (mSSC) play a role in tendon-to-bone healing after partial-injury. Using fluorescence-activated cell sorting we identified that found that they are present within the TBI. Using a TBI-injury rainbow lineage tracing mouse model, we demonstrated that injury-responsive cells within the TBI and calcaneus proliferate polyclonally following partial-tendon injury at the TBI. These injury-responsive clonal cells express skeletal marker SP7. We quantified the differences in mSCC frequency after TBI-injury and found that mSSC respond to injury with a higher frequency and have associated changes in gene expression, with the specific down-regulation of the TGFβ signaling pathway. Exogenous delivery of TGFβ after injury was found to reduce the mSSC response after injury. These findings suggest that mSSC may facilitate tendon-to-bone healing by downregulating TGFβ signaling within the mSSC niche.

2022-02-14 | GSE167080 | GEO

Partial Tendon Injury at the Tendon-to-Bone Enthesis Activates Skeletal Stem Cells

Project description:Partial Tendon Injury at the Tendon-to-Bone Enthesis Activates Skeletal Stem Cells

| PRJNA719822 | ENA

Transcription profiling of mouse embryonic fibroblasts from wild type and IRAK-4 kinase dead animals stimulated with IL-1b for different durations to identify IRAK-4 kinase-dependent IL-1b response genes.

Project description:IRAK-4 is an essential component of the signal transduction complex downstream of the IL-1- and Toll-like receptors. Though regarded as the first kinase in the signaling cascade, the role of IRAK-4 kinase activity versus its scaffold function is still controversial. In order to investigate the role of IRAK-4 kinase function in vivo, knock-in mice were generated by replacing the wild type IRAK-4 gene with a mutant gene encoding kinase deficient IRAK-4 protein (IRAK-4 KD). Analysis of embryonic fibroblasts and macrophages obtained from IRAK-4 KD mice with a number of experimental techniques demonstrated that they greatly lack responsiveness to stimulation with IL-1b or a Toll-like receptor 7 (TLR7) agonist. One of the techniques used, microarray analysis, identified IRAK-4 kinase-dependent IL-1b response genes in mouse embryonic fibroblasts and revealed that the induction of IL-1b-responsive mRNAs was largely ablated in IRAK-4 KD cells. In summary, our results suggest that IRAK-4 kinase activity plays a critical role in IL-1R/TLR7-mediated induction of inflammatory responses. Experiment Overall Design: The response of mouse embryonic fibroblasts from WT and IRAK4 kinase dead animals to stimulation with IL-1b at two time points was determined. There were 12 samples in total, 6 from WT and 6 from IRAK4 kinase dead cells; for each strain there were 3 conditions: growth for 4 hours without stimulation (the strain-specific control), growth for 1 hour with stimulation, and growth for 4 hours with stimulation; for each condition there were two biological replicates.

2007-11-15 | E-GEOD-6789 | biostudies-arrayexpress

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