Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cardiovascular risk in patients with type 2 diabetes is associated with alteration of blood monocyte phenotype and plasma metabolome

ABSTRACT: To gain insight into the relationship between circulating monocytes and cardiovascular risk (CV) progression in patients with type 2 diabetes (T2D), we collected blood monocytes (CD14 positive selection) from 92 people with type 2 diabetes and coronary artery calcium score (CAC-score). Gene expression profiles of circulating monocytes were assessed by RNA sequencing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE201087 | GEO | 2024/01/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

Identified differentially expressed lncRNAs in type 2 diabetes patients

Project description:Long noncoding RNAs (lncRNAs) is already evidently involved in a variety of biological functions and pathophysiological mechanisms underlying the diabetes. However, the role of lncRNAs in the type 2 diabetes (T2D) has not been explored clearly yet. The aim of this study was to determine the circulating lncRNA profile and confirmed the differentially expressed lncRNA between T2D patients.

2020-06-30 | GSE134594 | GEO

Profiling of CD14+ monocytes from humans with Type diabetes and without diabetes [RNA-Seq]

Project description:Monocyte activation by high glucose and free fatty acids promotes inflammation implicated in vascular complications associated with Type 2 diabetes (T2D). Emerging evidence shows that long non coding RNA (lncRNA)s regulate inflammation, but their role in T2D induced monocyte dysfunction is unclear. To examine this, we profiled the transcriptome of CD14+ monocytes from volunteers with T2D and without diabetes (n=5 each) using strand-specific RNA-seq on Illumina HiSeq 2500. Our study identified several differentially regulated lncRNAs along with coding genes involved in monocyte functions related to inflammation and monocytosis.

2021-06-23 | GSE156061 | GEO

Single-cell analysis of human PBMCs in healthy and type 2 diabetes populations: Dysregulated immune networks in type 2 diabetes unveiled through single-cell profiling

Project description:Abnormalities in glucose metabolism that precede the onset of type 2 diabetes (T2D) activate immune cells, leading to elevated inflammatory factors and chronic inflammation. However, no single-cell RNA sequencing (scRNA-seq) studies have characterized the properties and networks of individual immune cells in T2D. Here, we analyzed peripheral blood mononuclear cells (PBMCs) from healthy controls and T2D patients by scRNA-seq. We found that CD14 monocytes in T2D patients were in a pro-inflammatory state and intermediate monocytes expressed more MHC class II genes. In T2D patients, cytotoxic CD4 T cells, effector memory CD8 T cells, and γδ T cells have increased cytotoxicity and clonal expansion. B cells were characterized by increased differentiation into intermediate B cells, plasma cells, and isotype class switching with increased expression of soluble antibody genes. These results suggest that monocytes, T cells, and B cells could interact to induce chronic inflammation in T2D patients with pro-inflammatory characteristics.

2024-06-12 | GSE268210 | GEO

Expansion of Islet-Resident Macrophages Leads to Inflammation Affecting Beta Cell Proliferation and Function in Obesity

Project description:Inflammation is a key component of the pathogenesis of obesity-associated type 2 diabetes (T2D). However, the nature of T2D-associated islet inflammation and its impacts on T2D-associated beta cell abnormalities remain poorly defined. Using both diet-induced and genetically modified T2D animal models, we explore immune components of islet inflammation and define their roles in regulating beta cell function and proliferation. Our studies show that T2D-associated islet inflammation is uniquely dominated by macrophages, without the involvement of adaptive immune cells. We identify two islet macrophage populations, characterized by their distinct phenotypes, anatomical distributions and functional properties. Obesity induces a local expansion of intra-islet macrophages, independent of the replenishment from circulating monocytes. In contrast, the abundance of peri-islet macrophages is negligibly affected by obesity. Functionally, intra-islet macrophages impair beta cell function in a cell-cell contact dependent manner. In contrast, both intra- and peri-islet macrophage populations are able to promote beta cell proliferation. Together, these data provide a definitive view of the genesis of T2D-associated islet inflammation and define specific roles of islet macrophages in regulating beta cell function and proliferation.

2019-01-02 | GSE112002 | GEO

Circulating isomiRs May Be Superior Biomarkers Compared to Their Corresponding Canonical miRNAs: A Pilot Biomarker Study of Using isomiR-ome to Detect Coronary Calcium-Based Cardiovascular Risk in Patients with NAFLD

Project description:Cardiovascular (CV) disease is the leading cause of morbidity and mortality in patients with non-alcoholic fatty liver disease (NAFLD). Yet clinically, distinguishing between NAFLD patients with average CV risk from those at elevated risk is not easily achieved by traditional CV risk factors and clinically-based scoring systems. Here we hypothesize that in-depth analysis of circulating miRNAs can identify strong putative biomarkers for the degree of CV risk among patients with NAFLD

2024-01-06 | GSE199533 | GEO

Transcriptome Alteration in the Diabetic Heart by Rosiglitazone: Implications for Cardiovascular Mortality

Project description:The type 2 diabetes medication, rosiglitazone, has come under scrutiny for possibly increasing the risk of cardiac disease and death. To investigate the effects of rosiglitazone on the diabetic heart, we performed cardiac transcriptional profiling of a murine model of type 2 diabetes, the C57BL/KLS-leprdb/leprdb (db/db) mouse. We compared cardiac gene expression profiles from three groups: untreated db/db mice (db-c), db/db mice after rosiglitazone treatment (db-t), and non-diabetic db/+ mice. Mice were divided into three groups: Non-diabetic controls (db/+), untreated diabetic controls (db-c), and rosiglitazone-treated diabetic mice (db-t). Whole-heart RNA from five mice from each of the three groups after four months with or without treatment was used for microarray analysis.Universal Reference RNAs for mouse (Stratagene, La Jolla, CA) were purchased as microarray reference controls.

2012-03-28 | E-GEOD-36875 | biostudies-arrayexpress

A Broad Network of Dysregulated Protein Phosphorylation Underlies Muscle Insulin Resistance in Type 2 Diabetes

Project description:Skeletal muscle insulin resistance is the earliest defect in type 2 diabetes (T2D), preceding and predicting disease development. Whether this represents the underlying primary defect in T2D or effects of changes in hormones or circulating metabolites is unknown. To address this question, we have developed a “disease-in-a-dish” model by differentiating iPS cells from T2D patients and controls into myoblasts (iMyo) and studied their function in vitro. We find that T2D iMyos exhibit multiple defects mirroring human disease including altered insulin signaling through the IRS/AKT pathway, decreased insulin-stimulated glucose uptake, and reduced mitochondrial oxidation. In addition, using global phosphoproteomics we find that T2D alters phosphorylation of a large network of targets of mTOR, S6K, PKC and other kinases including proteins involved in regulation of Rho-GTPases, mRNA splicing/processing, vesicular trafficking, gene transcription and chromatin remodeling. This cell-autonomous dysregulated phosphorylation network reveals a new dimension in the mechanism underlying insulin resistance in T2D.

2020-08-27 | PXD015430 | Pride

Phenylalanine Impairs Insulin Signaling and Inhibits Glucose Uptake Through Modification of IRβ

Project description:Whether amino acids act on cellular insulin signaling remains unclear, given that increased circulating amino acid levels are associated with the onset of type 2 diabetes (T2D). Here, we report that phenylalanine modifies insulin receptor beta (IRβ) and inactivates insulin signaling and glucose uptake. Mice fed phenylalanine-rich chow or phenylalanine-producing aspartame or overexpressing human phenylalanyl-tRNA synthetase (hFARS) developed insulin resistance and T2D symptoms. Mechanistically, FARS phenylalanylated lysine 1057/1079 of IRβ (F-K1057/1079), inactivating IRβ and preventing insulin from promoting glucose uptake by cells. SIRT1 reversed F-K1057/1079 and counteracted the insulin-inactivating effects of hFARS and phenylalanine. F-K1057/1079 and SIRT1 levels in white blood cells from T2D patients wereare positively and negatively correlated with T2D onset, respectively. Blocking F-K1057/1079 with phenylalaninol sensitizeds insulin signaling and relieveds T2D symptoms in hFARS-transgenic and db/db mice. These findings shed light on the activation of insulin signaling and T2D progression through inhibition of phenylalanylation.

2022-07-22 | PXD035076 | Pride

Transcriptome Alteration in the Diabetic Heart by Rosiglitazone: Implications for Cardiovascular Mortality

2012-03-29 | GSE36875 | GEO

RNA-sequencing of IRF5+ and IRF5- circulating monocytes from patients with Type-2 Diabetes

Project description:Purpose: To characterise the transcriptomic landscape in monocytes associated with IRF5 expression Methods: RNA sequencing from FACS sorted IRF5+ and IRF5- CD14+ monocytes Results: Differential expression based on IRF5 postiivity provides insight into its roles in monocyte function and in type-2 diabetes Conclusions: This study represents the first analyses of IRF5-dependent transcriptome in circulating monocytes from patients with Type-2 diabetes

2022-07-22 | GSE176216 | 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