Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The study of inflammatory responses in mammalian macrophages with LPS stimulation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE76563 | GEO | 2016/02/24

SECONDARY ACCESSION(S): PRJNA307977

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The study of inflammatory responses in mammalian macrophages with LPS stimulation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-02-24 | E-GEOD-76563 | biostudies-arrayexpress

MK2 and MK3 regulate LPS-induced inflammatory response of macrophages

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

2019-07-30 | GSE123043 | GEO

Titanium induces pro-inflammatory and tissue remodeling responses in human macrophages

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

2021-02-10 | GSE99448 | GEO

Endothelial in vivo vs. in vitro responses to LPS

Project description:Endothelial responses to LPS using endothelial cells freshly isolated from Tie2 GFP animals vs. cultured cell line. This SuperSeries is composed of the SubSeries listed below.

2010-06-09 | E-GEOD-1044 | biostudies-arrayexpress

Nanotoxicogenomic study of ZnO and TiO2 responses

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-07-25 | E-GEOD-39444 | biostudies-arrayexpress

Genome-wide siRNA screen of genes regulating the Lipopolysaccharide-induced responses in mammalian macrophages

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

2017-02-23 | GSE83826 | GEO

Juglone Suppresses LPS-induced Inflammatory Responses and NLRP3 Activation in Macrophages.

Project description:The NLRP3 (NACHT, LRR and PYD domains-containing protein 3) inflammasome has been implicated in a variety of diseases, including atherosclerosis, neurodegenerative diseases, and infectious diseases. Thus, inhibitors of NLRP3 inflammasome have emerged as promising approaches to treat inflammation-related diseases. The aim of this study was to explore the effects of juglone (5-hydroxyl-1,4-naphthoquinone) on NLRP3 inflammasome activation. The inhibitory effects of juglone on nitric oxide (NO) production were assessed in lipopolysaccharide (LPS)-stimulated J774.1 cells by Griess assay, while its effects on reactive oxygen species (ROS) and NLRP3 ATPase activity were assessed. The expression levels of NLRP3, caspase-1, and pro-inflammatory cytokines (IL-1β, IL-18) and cytotoxicity of juglone in J774.1 cells were also determined. Juglone was non-toxic in J774.1 cells when used at 10 μM (p < 0.01). Juglone treatment inhibited the production of ROS and NO. The levels of NLRP3 and cleaved caspase-1, as well as the secretion of IL-1β and IL-18, were decreased by treatment with juglone in a concentration-dependent manner. Juglone also inhibited the ATPase activities of NLRP3 in LPS/ATP-stimulated J774.1 macrophages. Our results suggested that juglone could inhibit inflammatory cytokine production and NLRP3 inflammasome activation in macrophages, and should be considered as a therapeutic strategy for inflammation-related diseases.

| S-EPMC7412499 | biostudies-literature

Histone deacetylase 2 is essential for LPS-induced inflammatory responses in macrophages.

Project description:The role of specific histone deacetylase (HDAC) proteins in regulating the lipopolysaccharide (LPS)-induced inflammatory response and its underlying mechanisms are unclear. Here, HDAC2, a class I HDAC family protein, is essential for the LPS-triggered inflammatory response in macrophages. LPS stimulation increases HDAC2 expression in macrophages. Knockdown of HDAC2 decreases the expression of proinflammatory genes, such as IL-12, TNF-α and iNOS following stimulation with LPS. The adoptive transfer of HDAC2 knockdown macrophages attenuates the LPS-triggered innate inflammatory response in vivo, and these mice are less sensitive to endotoxin shock and Escherichia coli-induced sepsis. Mechanistically, the c-Jun protein is the main target of HDAC2-mediated LPS-induced production of proinflammatory cytokines. Moreover, HDAC2 knockdown increases the expression of c-Jun, which directly binds the promoters of proinflammatory genes and forms nuclear receptor corepressor complexes to inhibit the transcription of proinflammatory genes in macrophages. These effects are rescued by c-Jun expression. According to the chromatin immunoprecipitation analysis, HDAC2 also selectively suppresses c-Jun expression by directly binding to its promoter and modifying histone acetylation after LPS stimulation. Our findings define a new function and mechanism of the HDAC2/c-Jun signaling network that regulates the LPS-induced immune response in macrophages.

| S-EPMC7379312 | biostudies-literature

Cross-species transcriptional network analysis defines shared inflammatory responses in murine and human lupus nephritis

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2012-12-10 | E-GEOD-37463 | biostudies-arrayexpress

Tristraprolin regulates basophil inflammatory responses

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

2024-11-17 | GSE272533 | GEO