Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Serum amyloid and serum amyloid P are not induced in response to diesel exhaust particles or carbon black

ABSTRACT: W evaluated an experimental particle exposure model, including markers of the acute phase system assessed as the hepatic mRNA expression of Sap, the murine homologue of CRP, and Saa1 and Saa3. Keywords: Toxicology, disease state analysis, stress response, nanoparticles, air pollution

ORGANISM(S): Mus musculus

PROVIDER: GSE11346 | GEO | 2009/04/27

SECONDARY ACCESSION(S): PRJNA106561

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of mouse Apoe knockouts treated with SRM2975 and C57Bl/6 mice treated with exhaust particles reveals Serum amyloid and serum amyloid P are not induced in response to diesel exhaust particles or carbon black

Project description:W evaluated an experimental particle exposure model, including markers of the acute phase system assessed as the hepatic mRNA expression of Sap, the murine homologue of CRP, and Saa1 and Saa3. Experiment Overall Design: 12-13 weeks old Apoe knockout mice (C57BL/6-Apoe tm1) mice were injected intraperitoneally with varying doses of SRM 2975. In a parallel experiment C57BL mice were exposed by inhalation for 90 minutes to four consecutive doses of 20mg/m3 of filtered air, NIST 2975 or Ptintex 90. Livers and aortic tissue were collected.

2009-05-02 | E-GEOD-11346 | biostudies-arrayexpress

Lung cell responses to ship diesel exhaust particles

2015-02-01 | GSE63962 | GEO

Lung cell responses to ship diesel exhaust particles

Project description:Human BEAS-2B bronchial epithelial cells were exposed directly at the air-liquid interphase towards exhaust gas and particles of a ship engine. The goal was to compare the responses towards different fuel combustions. The engine run either on diesel fuel (DF) or on Heavy Fuel Oil (HFO). The lung cells were exposed 3 times to each combustion aerosol (DF or HFO). The duration of the exposure was 4h. The cells were seeded into transwell-inserts 24h before exposure. Within each exposure 3 transwell-inserts were exposed to the complete aerosol and 3 transwell-inserts were exposed to the filtered aerosol. Effects of the complete aerosol were referenced against the filtered aerosol to determine the effects of the aerosol particles.

2015-02-01 | E-GEOD-63962 | biostudies-arrayexpress

Effects of Diesel Exhaust Particles on Mouse Gastric Stem Cells.

Project description: Not available

| S-EPMC7460091 | biostudies-literature

Diesel exhaust particles override natural injury-limiting pathways in the lung.

Project description: Not available

| S-EPMC2928610 | biostudies-literature

Lack of acute phase response in the livers of mice exposed to diesel exhaust particles or carbon black by inhalation.

Project description: Not available

| S-EPMC2673201 | biostudies-literature

Effect of serum amyloid A1 (SAA1) on gene expression in primary murine macrophages

Project description:Macrophages are important regulators of the immune system and are critically involved in the pathophysiology of many diseases. Serum amlyoidosis is a protein misfolding disease which can follow chronic inflammatory conditions. Deposition of fibrils formed from serum amyloid A1 (SAA1) protein occurs systemically and can lead to severe or even fatal outcomes. Macrophages play a critical role in the misfolding and deposition of SAA1-derived fibrils and the role of macrophages in this context has been studied extensively. It is known that SAA1 can bind to some surface receptors on macrophages and it is taken up by the macrophages and metabolized in the lysosomes. On the other hand, the effect of SAA1 on macrophage physiology has been much less investigated so far. Therefore, we aim to investigate the effect of SAA1 on macrophage gene expression by gene microarray analysis. To this end, primary peritoneal macrophages from NMRI mice were treated with endotoxin-free recombinantly expressed full-length mSAA1 for 6 and 24 h and gene expression was analyzed.

2021-07-20 | GSE155278 | GEO

Protein kinase C-? mediates lung injury induced by diesel exhaust particles.

Project description: Not available

| S-EPMC3604088 | biostudies-other

RNA sequencing of sorted cells from mouse PDAC

Project description:Pancreatic ductal adenocarcinoma (PDAC) is characterized by the presence of abundant desmoplatic stroma primarily composed of cancer-associated fibroblasts (CAFs). It is generally accepted that CAFs stimulate tumor progression and might be implicated in drug resistance and immunosuppression. Here, we have compared the transcriptional profile of PDGFRα+ CAFs isolated from genetically engineered mouse PDAC tumors with that of normal pancreatic fibroblasts (NPFs) to identify genes potentially implicated in their pro-tumorigenic properties. We report that the most differentially expressed gene, Saa3, a member of the acute-phase Serum Amyloid A (SAA) apolipoprotein family, is a key mediator of the pro-tumorigenic activity of PDGFRα+ CAFs. Whereas Saa3 competent CAFs stimulate the growth of PDAC tumor cells in an orthotopic model, Saa3 null CAFs inhibit tumor growth. Saa3 also plays a role in the cross-talk between CAFs and tumor cells. Ablation of Saa3 in pancreatic tumor cells makes them insensitive to the inhibitory effect of Saa3 null CAFs. As a consequence, germline ablation of Saa3 does not prevent PDAC tumor development in mice. The pro-tumorigenic activity of Saa3 in CAFs is mediated by Mpp6, a member of the palmitoylated membrane protein subfamily of the peripheral membrane-associated guanylate kinases. Finally, we interrogated whether these observations could be translated to a human scenario. Indeed, SAA1, the orthologue of murine Saa3, is overexpressed in human CAFs. Moreover, high levels of SAA1 in the stromal component correlate with worse survival. These findings support the concept that selective inhibition of SAA1 in CAFs may provide potential therapeutic benefit to PDAC patients.

2018-01-22 | GSE106901 | GEO

In vitro transformation of human bronchial epithelial cells by diesel exhaust particles

Project description:The potential of diesel exhaust particles (DEP) to transform human bronchial epithelial cells (HBEC3) was investigated and a stably transformed cell line (T2-HBEC3) was established. Short-term DEP exposure experiments adds information of immunomodulatory effect markers and differences in susceptibility between normal and sensitized bronhial epithelial cells of the human lung.

2017-11-30 | GSE107481 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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