Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Regulation of succinate signaling and immunometabolism in diabetes-associated atherosclerosis by miR-369-3p

ABSTRACT: Regulation of succinate signaling and immunometabolism in diabetes-associated atherosclerosis by miR-369-3p

PROVIDER: PRJNA1024509 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26297607_1.fastq.gz	Fastqsanger.gz
	SRR26297607_2.fastq.gz	Fastqsanger.gz
	SRR26297608_1.fastq.gz	Fastqsanger.gz
	SRR26297608_2.fastq.gz	Fastqsanger.gz
	SRR26297609_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Regulation of succinate signaling and immunometabolism in diabetes-associated atherosclerosis by miR-369-3p

Project description:Atherosclerosis is accelerated under diabetic conditions in part due to altered macrophage metabolism and function. Identifying critical factors to restore metabolic alterations and promote resolution of inflammation remains an unmet goal. MicroRNAs (miRs) orchestrate multiple signaling events in macrophages and regulate inflammation, yet their therapeutic potential in diabetes-associated atherosclerosis remains poorly understood. miRNA profiling of aortic intimal lesions from Ldlr-/- mice on a high-fat sucrose containing (HFSC) diet for 12 weeks revealed low expression of miR-369-3p. miR-369-3p was also reduced in peripheral blood mononuclear cells (PBMCs) from diabetic patients with coronary artery disease. Cell-type expression profiling showed miR-369-3p enrichment in aortic macrophages. Treatment with oxLDL reduced miR-369-3p expression in-stimulation mouse bone marrow-derived macrophages (BMDMs) downregulated miR-369-3p. Overexpression of miR-369-3p restored the oxLDL-mediated decrease of OXPHOS in BMDMs. Mechanistically, we found that miR-369-3p targeted the succinate receptor (GPR91) to alleviate the oxLDL-induced activation of inflammasome signaling pathways. Therapeutic administration of miR-369-3p in HFSC-fed Ldlr-/- mice reduced GPR91 expression in lesional macrophages and the diabetes-mediated accelerated atherosclerosis, evident by a decrease in plaque size and in the accumulation of pro-inflammatory Ly6Chi macrophages. RNA-seq analyses showed more pro-resolving pathways in plaque macrophages from miR-369-3p treated mice, consistent with an increase in macrophage efferocytosis in lesions. These findings establish a therapeutic role for miR-369-3p in halting diabetes-associated atherosclerosis by regulating GPR91 and macrophage succinate metabolism.

2024-12-04 | GSE244760 | GEO

Anti-influenza activity of succinate

Project description:In the present study, we discovered an unexpected interplay between immunometabolism and antiviral immunity. Profiling of human bronchial epithelial BEAS-2B cells was performed using Agilent’s SurePrint G3 human gene expression microarray kit. A single-color design provided two types of comparison: (i) IAV-infected versus mock-infected cells, and (ii) succinate-treated infected cells versus mock-infected cells.

2022-02-17 | E-MTAB-10031 | biostudies-arrayexpress

Consotaella salsifontis strain:USBA 369 | isolate:CMPUJ U 369

Project description:Consotaella salsifontis strain:USBA 369 | isolate:CMPUJ U 369 Genome sequencing

| PRJNA329801 | ENA

Variovorax sp. 369

Project description:Variovorax sp. 369 Genome sequencing and assembly

| PRJNA509336 | ENA

Effect of miR-92a-3p and/or miR-489-3p inhibition on aorta endothelium of Apoe-/-;5/6Nx

Project description:The role of endothelial miR-92a-3p and miR-489-3p in CKD-associated atherosclerosis was examined by mRNA expression analysis in Apoe-/- mice with 5/6 nephrectomy treated with locked-nucleic acid (LNA) inhibitors complexed with high-density lipoprotein (HDL).

2019-03-01 | GSE120038 | GEO

Caldimonas manganoxidans ATCC BAA-369

Project description:Caldimonas manganoxidans ATCC BAA-369

| PRJNA182454 | ENA

Saccharum robustum cultivar:IJ76-369

Project description:Saccharum robustum IJ76-369 Resequencing

| PRJNA1228915 | ENA

Panicum virgatum cultivar:SPR-369

Project description:Panicum virgatum exome capture - SPR-369

| PRJNA446214 | ENA

miRNA expression profiling of murine LPS-stimulated dendritic cells exposed to quercetin

Project description:Dendritic cells (DCs) are the most potent antigen-presenting cells that play an important role in the crosstalk between the innate and the adaptive immune response. We identified quercetin exposure as an effective strategy to suppress DCs inflammatory response induced by LPS. In this study, using NGS analysis, we examined the effect of quercetin on miRNAs expression in DCs. We defined a signature of 113 miRNAs differentially regulated in LPS-stimulated DCs after quercetin exposure. Among them, we observed an upregulation of miR-369-3p that potentially regulated C/EBP-beta. We functionally demonstrate that the loss of function of miR-369-3p in LPS-stimulated DCs during quercetin exposure led to an increase of C/EBP-beta and its downstream targets TNFα and IL6. Conversely, we showed that the ectopic induction of miR-369-3p even without quercetin suppresses the inflammatory response of LPS reducing C/EBP-beta, TNFα and IL6 production. In vivo, oral administration of quercetin induces miR-369-3p expression. These data demonstrate that a key mediator of immunosuppressive effect of quercetin is miR-369-3p. These findings could have potentially therapeutic implications since the induction of miR-369-3p expression may have anti-inflammatory effect.

2019-12-31 | GSE112327 | GEO

Succinate dehydrogenase deficiency-driven succinate accumulation induces drug resistance in acute myeloid leukemia via ubiquitin-cullin regulation

Project description:Drug resistance is vital for the poor prognosis of acute myeloid leukemia (AML) patients, but the underlying mechanism remains poorly understood. Given the unique microenvironment of bone marrow, we reasoned that drug resistance of AML might rely on distinct microenvironment-associated metabolic processes. Here, we identified SDH deficiency and over-cumulative succinate as typical features in AML, with a marked function in causing the resistance of AML cells to a wide range of anti-cancer therapies. Mechanistically, succinate promoted the accumulation of oncogenic proteins in a manner that precedes transcriptional activation. This function was mediated by succinate-triggered upregulation of UBC12 phosphorylation, which impaired its E2 function in cullins neddylation. Notably, decreasing succinate levels by fludarabine could effectively restore the drug sensitivity of SDH-deficient AML PDX. Together, we uncover a novel function of succinate in driving drug resistance by regulating p-UBC12/cullin activity, and indicate reshaping succinate metabolism as a promising treatment for SDH-deficient AML.

2024-08-27 | GSE247623 | 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