Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of PGC-1beta deficiency, or LPS or IFN-beta activation, on gene expression of bone marrow-derived dendritic cells

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

ORGANISM(S): Mus musculus

PROVIDER: GSE204957 | GEO | 2022/05/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of PGC-1beta deficiency, or LPS or IFN-beta activation, on gene expression of bone marrow-derived dendritic cells

Project description:Effect of PGC-1beta deficiency, or LPS or IFN-beta activation, on gene expression of bone marrow-derived dendritic cells

| PRJNA842766 | ENA

Effect of PGC-1beta deficiency on gene expression of bone marrow-derived dendritic cells

Project description:To determine the changes in gene expression regulated by PGC-1beta, we knocked down PGC-1beta in bone marrow-derived dendritic cells by shRNA.

2022-05-29 | GSE204954 | GEO

Effect of LPS or IFN-beta activation on gene expression of bone marrow-derived dendritic cells

Project description:To examine the changes in genes encoding proteins of metabolic pathways induced by LPS or IFN-beta in bone marrow-derived dendritic cells.

2022-05-29 | GSE204955 | GEO

Effect of PGC-1beta deficiency on gene expression of bone marrow-derived dendritic cells

Project description:Effect of PGC-1beta deficiency on gene expression of bone marrow-derived dendritic cells

| PRJNA842772 | ENA

Effect of LPS or IFN-beta activation on gene expression of bone marrow-derived dendritic cells

Project description:Effect of LPS or IFN-beta activation on gene expression of bone marrow-derived dendritic cells

| PRJNA842771 | ENA

Bone Marrow-Derived Dendritic Cell Cultures from RAG<sup>-/-</sup> Mice Include IFN-γ-Producing NK Cells.

Project description:Dendritic cells (DCs) play a key role in the initiation of an immune response and are known as "professional" APCs because of their ability to activate naive T cells. A widely used method to generate DCs in vitro is to culture bone marrow (BM) cells or blood monocytes in the presence of GM-CSF and IL-4. In this study, we show that a small population of NK cells residing in the BM of RAG-/-, but not RAG-/- γc chain-/- mice, remain in the DC culture and is the source of IFN-γ produced after stimulation with LPS. These cells, which may represent early promoters of LPS-induced responses, have to be taken into account when interpreting experiments using BM-derived DCs.

| S-EPMC7454002 | biostudies-literature

Oxidative stress causes bone loss in estrogen-deficient mice through enhanced bone marrow dendritic cell activation.

Project description:Increased production of tumor necrosis factor alpha (TNF) in the bone marrow (BM) in response to both oxidative stress and T cell activation contributes to the bone loss induced by estrogen deficiency, but it is presently unknown whether oxidative stress causes bone loss through T cells. Here we show that ovariectomy causes an accumulation in the BM of reactive oxygen species, which leads to increased production of TNF by activated T cells through up-regulation of the costimulatory molecule CD80 on dendritic cells. Accordingly, bone loss is prevented by treatment of ovariectomized mice with either antioxidants or CTLA4-Ig, an inhibitor of the CD80/CD28 pathway. In summary, reactive oxygen species accumulation in the BM is an upstream consequence of ovariectomy that leads to bone loss by activating T cells through enhanced activity of BM dendritic cells, and these findings suggest that the CD80/CD28 pathway may represent a therapeutic target for postmenopausal bone loss.

| S-EPMC1986617 | biostudies-literature

Biomechanical forces enhance directed migration and activation of bone marrow-derived dendritic cells.

Project description:Mechanical forces are pervasive in the inflammatory site where dendritic cells (DCs) are activated to migrate into draining lymph nodes. For example, fluid shear stress modulates the movement patterns of DCs, including directness and forward migration indices (FMIs), without chemokine effects. However, little is known about the effects of biomechanical forces on the activation of DCs. Accordingly, here we fabricated a microfluidics system to assess how biomechanical forces affect the migration and activity of DCs during inflammation. Based on the structure of edema, we proposed and experimentally analyzed a novel concept for a microchip model that mimicked such vascular architecture. The intensity of shear stress generated in our engineered chip was found as 0.2-0.6 dyne/cm2 by computational simulation; this value corresponded to inflammation in tissues. In this platform, the directness and FMIs of DCs were significantly increased, whereas the migration velocity of DCs was not altered by shear stress, indicating that mechanical stimuli influenced DC migration. Moreover, DCs with shear stress showed increased expression of the DC activation markers MHC class I and CD86 compared with DCs under static conditions. Taken together, these data suggest that the biomechanical forces are important to regulate the migration and activity of DCs.

| S-EPMC8187447 | biostudies-literature

Biomechanical forces enhance directed migration and activation of bone marrow-derived dendritic cells.

| S-EPMC8187447 | biostudies-literature

Liver-specific PGC-1beta deficiency leads to impaired mitochondrial function and lipogenic response to fasting-refeeding.

Project description:PGC-1? plays pleiotropic roles in regulating intermediary metabolism and has been shown to regulate both catabolic and anabolic processes in liver. We sought to evaluate the effects of PGC-1? on liver energy metabolism by generating mice with postnatal, liver-specific deletion of PGC-1? (LS-PGC-1?(-/-) mice). LS-PGC-1?(-/-) mice were outwardly normal, but exhibited a significant increase in hepatic triglyceride content at 6 weeks of age. Hepatic steatosis was due, at least in part, to impaired capacity for fatty acid oxidation and marked mitochondrial dysfunction. Mitochondrial DNA content and the expression of genes encoding multiple steps in mitochondrial fatty acid oxidation and oxidative phosphorylation pathways were significantly diminished in LS-PGC-1?(-/-) mice. Liquid chromatography mass spectrometry-based analyses also revealed that acetylcarnitine and butyrylcarnitine levels were depleted whereas palmitoylcarnitine content was increased in LS-PGC-1?(-/-) liver, which is consistent with attenuated rates of fatty acid oxidation. Interestingly, loss of PGC-1? also significantly impaired inducible expression of glycolytic and lipogenic enzymes that occurs with high carbohydrate diet refeeding after a prolonged fast. These results suggest that PGC-1? plays dual roles in regulating hepatic fatty acid metabolism by controlling the expression of programs of genes involved in both fatty acid oxidation and de novo fatty acid synthesis.

| S-EPMC3532159 | biostudies-literature

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