Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Diabetes accelerates atherosclerosis through lactate induced GPR132-Src activation

ABSTRACT: Diabetes accelerates atherosclerosis through lactate induced GPR132-Src activation

PROVIDER: PRJNA1138244 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29904352_1.fastq.gz	Fastqsanger.gz
	SRR29904352_2.fastq.gz	Fastqsanger.gz
	SRR29904353_1.fastq.gz	Fastqsanger.gz
	SRR29904353_2.fastq.gz	Fastqsanger.gz
	SRR29904354_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Diabetes accelerates atherosclerosis through lactate induced GPR132-Src activation

Project description:Diabetes mellitus is one of the major independent risk factors for the development of ASCVD. Several studies have reported that diabetes increases inflammatary signaling in different cells, and the cytokines may influence plaque formation, but the signal pathway in circulating cells that links glucose metabolism and lipid metabolism remains unclear.We isolated peritoneal macrophages of diabetic and non-diabetic APOE-/- mice to investigate the diabetes influence on macrophages.

2025-03-01 | GSE272712 | GEO

Neutrophil Extracellular Traps (NETs) promote macrophage inflammation and impair atherosclerosis resolution in mice with diabetes

Project description:Neutrophil extracellular traps (NETs) promote inflammation and atherosclerosis progression. In diabetes they are increased and impair wound healing, during which inflammation normally resolves. Atherosclerosis regression, a process resembling wound healing, is also impaired in diabetes. Thus, we hypothesized that NETs impede atherosclerosis regression in diabetes through unresolved inflammation. Objective: To investigate in diabetes the effect of NETs on plaque macrophage inflammation and whether NETs reduction improves atherosclerosis regression. Findings: Transcriptomic profiling of plaque macrophages from NET positive and negative areas in Ldlr-/- mice revealed inflammasome and glycolysis pathway upregulation, indicating a pro-inflammatory phenotype. During atherosclerosis regression in non-diabetic mice, plaque NET content decreased. In contrast, in diabetic mouse plaques NETs were enriched and persisted after lipid-lowering. DNase1 treatment (to degrade NETs) of diabetic mice reduced plaque NETs and macrophage inflammation and improved atherosclerosis regression after lipid-lowering. Conclusions: NETs decline during atherosclerosis regression in non-diabetic mice, but persist in diabetes and impair regression by exacerbating macrophage inflammation. DNase1 reduced diabetic plaque NETs and macrophage inflammation, and restored atherosclerosis resolution after lipid-lowering, despite ongoing hyperglycemia. Given that humans with diabetes also exhibit impaired atherosclerosis resolution with lipid-lowering, these data suggest that NETs contribute to the increased CVD risk in this population.

2020-05-12 | GSE145200 | GEO

Intermittent childhood hyperlipidaemia alters resident arterial macrophages and accelerates atherosclerosis

Project description:Intermittent childhood hyperlipidaemia alters resident arterial macrophages and accelerates atherosclerosis

| PRJEB60746 | ENA

Intermittent childhood hyperlipidaemia alters resident arterial macrophages and accelerates atherosclerosis

Project description:Intermittent childhood hyperlipidaemia alters resident arterial macrophages and accelerates atherosclerosis

| PRJEB60780 | ENA

Genome-wide Profiling of SRC-2 (NCOA2) binding in mouse prostate [ChIP-Seq]

Project description:Using genetically engineered mice, overexpressing SRC-2, specifically in the prostate epithelium of PTEN heterozygous mice accelerates PTEN mutation induce tumor progression and develops a metastasis-prone cancer. Here we used ChIP-Seq analysis to identify genome-wide SRC-2 binding sites in mouse prostate. Examination of genome-wide SRC-2 binding in mouse prostate by ChIP-seq analysis. Samples were collected from pooled dorsal-lateral prostates of 7 months old-PTEN flox/+; Rosa26-SRC-2 OE/+ mice. Flash frozen tissues were then sent to Active Motif, Inc. for chromatin extraction and followed by immunoprecipitation using anti-SRC-2 antibody (A300-346A, Bethyl Lab., Inc.).

2014-06-30 | E-GEOD-54770 | biostudies-arrayexpress

A novel lesional transciptional signature separates atherosclerosis with and without diabetes in Yorkshire swine and humans

Project description:This study identifies evolutionarily conserved gene signatures and signaling pathways in a stage-specific manner that successfully distinguishes diabetes and non-diabetes-associated atherosclerosis. These findings establish new molecular insights and therapeutic opportunities to potentially control accelerated atherosclerotic lesion formation in diabetes.

2021-02-01 | GSE162391 | GEO

A pivotal role of SRC-2 in Metastatic and Castration Resistant Prostate Cancer

Project description:SRC-2 is frequently amplified or overexpressed in metastatic prostate cancer patients. In this study, we used genetically engineered mice, overexpressing SRC-2 specifically in the prostate epithelium as a mouse model to examine the role of SRC-2 in prostate tumorigenesis. Over-expression of SRC-2 in PTEN heterozygous mice accelerates PTEN mutation induced tumor progression and develops a metastasis-prone cancer. We used microarrays to examine the molecular profile of prostate-specific SRC-2 overexpression adult dorsal-lateral prostate in comparison with that of control PTENF/+ heterozygous deletion mice. Total RNA was extracted from dorsal-lateral prostate of 7 months old-PTEN flox/+ control and PTEN flox/+; Rosa26-SRC-2 OE/+ adult mice, followed by gene expression profiling using Affymetrix microarrays. Each sample contains pooled prostate RNA from 3 mice.

2014-06-30 | E-GEOD-54678 | biostudies-arrayexpress

Genome-wide Profiling of SRC-2 (NCOA2) binding in mouse prostate [ChIP-Seq]

2014-06-30 | GSE54770 | GEO

A pivotal role of SRC-2 in Metastatic and Castration Resistant Prostate Cancer

2014-06-30 | GSE54678 | GEO

The loss of CARMN regulates vascular smooth muscle cell phenotype and accelerates the development of atherosclerosis in mice.

Project description:We investigated the function of CARMN lncRNA, located immediately upstream of the miRNAs miR-143 and miR-145, as critical regulator of vSMC phenotypes in vitro and the consequence of its loss during the development of atherosclerosis in vivo. We hypothesized that loss of CARMN is a primary event controlling the functional switch towards pro-atherogenic vSMC phenotypes and accelerates the development of the plaques in vivo.

2021-04-06 | GSE158972 | 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