Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tubuloside B alleviates inflammation of murine macrophages

ABSTRACT: Purpose: Studies in mice have indicated that Tubuloside B has therapeutic potentials in various models of inflammatory diseases. We set out to analyze how Tubuloside B regulates transcription in LPS+IFN-γ-stimulated macrophages. Methods: RNA-seq was performed with two repetitions in RAW264.7 followed by treatment with Tubuloside B and LPS as well as IFN-γ. Conclusions: Tubuloside B inhibits the production of pro-inflammatory cytokines in activated macrophages.

ORGANISM(S): Mus musculus

PROVIDER: GSE155566 | GEO | 2021/07/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression profiles of M1-polarized RAW264.7 cells [RAW_M1vsM0_RNA-seq]

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to evaluate the gene expression of M1-polarized RAW264.7 cells compared with M0 RAW264.7 cells. Methods: RAW264.7 cells were polarized toward M1 using LPS and IFN-γ. M0 RAW264.7 cells were maintained in culture without LPS and IFN-γ. Total RNA of M1 and M0 RAW264.7 cells was extracted. RAW264.7 cells RNA profiles were generated by deep sequencing for two groups (M1 versus M0 RAW264.7 cells) with three samples each. Results: There were significant differences between M1 and M0 RAW264.7 cells. Conclusions: Polarization of RAW264.7 cells from M0 to M1 induces various changes at the transcription level.

2024-03-31 | GSE183077 | GEO

Widespread cysteine persulfidation in activated macrophages as a protective mechanism against oxidative-inflammatory stress

Project description:A hallmark of immune-inflammatory responses is the generation of reactive oxygen and nitrogen species by innate immune cells, in particular macrophages. How macrophages cope with excess oxidant production and associated redox stress is not fully understood. Recent evidence implicates reactive sulfur species (RSS) in inflammatory responses, however, how RSS affect macrophage function and its ability to cope with oxidative-inflammatory stress remains poorly understood. Herein, we investigated endogenous pathways of RSS biogenesis and clearance in macrophages, and in particular, explored how hydrogen sulfide (H2S) and thiol persulidation influences macrophage oxidative-inflammatory response. We report that classical activation of mouse or human macrophages with lipopolysaccharide and interferon-γ (LPS/IFN-γ) triggers a marked production of H2S/RSS, leading to a widespread increase in protein persulfidation. Endogenous H2S/persulfidation levels were governed by the activity of the cystine importer xCT, the H2S-generating enzyme cystathionine γ-lyase and the sulfide-metabolizing enzyme sulfide quinone oxidoreductase (SQOR). High levels of H2S/persulfidation, observed upon LPS/IFN-γ stimulation or SQOR inhibition, were associated with a state of increased resistance to oxidative stress. Furthermore, enhanced persulfidation correlated with attenuated activation of the macrophage inflammasome and diminished inflammatory cell death. These findings shed light on the metabolism and effects of RSS in macrophages and point to an important role for persulfides in enabling macrophages to cope with oxidative-inflammatory stress.

2024-05-21 | PXD044043 | Pride

Effect of Drp1 inhibitor on gene expression profiles of RAW264.7 cells at 24 hours or 96 hours after LPS and IFN-γ stimulation

Project description:Effects of Drp1 inhibitor Mdivi-1 on gene expression profiles of LPS and IFN-γ-treated RAW264.7 cells were examined.

2024-10-08 | GSE278583 | GEO

miRNA expression profiles of macrophages (cell line: RAW264.7) and endothelial cells (cell line: TIME)

Project description:We report the miRNA profiles of macrophages (cell line: RAW264.7) and endothelial cells (cell line: TIME) after supplementation with polyunsaturated fatty acids (PUFA) and stimulation with LPS/pro-inflammatory cytokines. The fatty acids docosahexaenoic acid (DHA, C22:6n3) or arachidonic acid (AA, C20:4n6) were included in the culture medium in concentrations of 15 µmol/L using ethanol as a vehicle (0.2 % v/v final ethanol concentration). Cells were cultured in the enriched media totaling either 72 h (RAW264.7) or 144 h (TIME). Stimulation of cells was performed in the last 24 h of fatty acid supplementation by addition of either LPS (1 µg/mL; from E. coli serotype 0111:B4) for cell line RAW264.7 or the cytokines IL-1β, TNF-α, and IFN-γ each in a concentration of 5 ng/ml for cell line TIME.

2019-08-22 | GSE132361 | GEO

IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate M1-like macrophage polarization [RNA-seq]

Project description:Complete polarization of macrophages towards an M1-like proinflammatory and antimicrobial state requires combined action of IFN-γ and LPS. Synergistic activation of canonical inflammatory NF-κB target genes by IFN-γ and LPS is well appreciated, but less is known about whether IFN-γ negatively regulates components of the LPS response, and how this affects polarization. A combined transcriptomic and epigenomic approach revealed that IFN-γ selectively abrogates LPS-induced feedback and select metabolic pathways by suppressing TLR4-mediated activation of gene enhancers. In contrast to superinduction of inflammatory genes via enhancers that harbor IRF sequences and bind STAT1, IFN-γ-mediated repression targeted enhancers with STAT sequences that bound STAT3. TLR4-activated IFN-γ-suppressed enhancers comprised two subsets distinguished by differential regulation of histone acetylation and recruitment of STAT3, CDK8 and cohesin, and were functionally inactivated by IFN-γ. These findings reveal that IFN-γ suppresses feedback inhibitory and metabolic components of the TLR response to achieve full M1 polarization, and provide insights into mechanisms by which IFN-γ selectively inhibits TLR4-induced transcription.

2019-06-12 | GSE120944 | GEO

IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate M1-like macrophage polarization [ChIP-seq]

2019-06-12 | GSE120943 | GEO

IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate M1-like macrophage polarization [ATAC-seq]

2019-06-12 | GSE120942 | GEO

IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate M1-like macrophage polarization [RNA-seq II]

2019-06-20 | GSE130567 | GEO

TMT-based quantitative MS analysis of proteome labeled by NO-responsive reaction with NOAR-2

Project description:RAW264.7 cells were treated by LPS and IFN-gamma for 20 h. The LPS/IFN treated or nontreated cells were labeled by NOAR-2 for 1 h. Cells were lysed by NP-40 buffer. Labeled proteins were purified by immunopecipitation using anti-fluorescein, then digested by trypsin. Digested peptides were labeled by TMTsixplex isobaric labeling reagents, followed by mass spectrometry measurement.

2020-01-12 | PXD012310 | JPOST Repository

Transcript dynamics in classically and alternatively activated macrophages

Project description:Using RNA-seq, we have reported that signaling crosstalk among IFN-γ and LPS is integrated at the level of transcriptome and have associated with TFs and TcoFs changes. In addition, we also argue that the transcriptional differences between BMDMs and RAW264.7 macrophage cell line as well as IL-4 and IL-13 on M2 macrophages activation.

2018-01-23 | GSE103958 | GEO

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