Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Human Circular RNA CircHMGCS1 Sponges miR-4521 to Aggravates Diabetes-Induced Vascular Endothelial Dysfunction Through Upregulating ARG1

ABSTRACT: Cardiovascular diseases pose a significant global health burden. Our study investigates the pivotal role of circular RNAs (circRNAs) and MicroRNAs (miRNAs) in diabetes-induced endothelial dysfunction, a critical aspect of cardiovascular diseases. CircHMGCS1 (hsa_circ_0008621) emerges as a specific circRNA that effectively targets miR-4521. The upregulation of CircHMGCS1 acts as a miR-4521 sponge, facilitating the expression of arginase 1 and accelerating the progression of diabetes-induced endothelial dysfunction. Furthermore, intricate associations among circRNA, miRNA, and mRNA are revealed, illuminating the underlying molecular mechanisms involved in diabetes-induced vascular endothelial dysfunction. These findings significantly advance our understanding of cardiovascular diseases, providing potential therapeutic targets for intervention.

ORGANISM(S): Homo sapiens

PROVIDER: GSE237597 | GEO | 2024/08/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The Circular RNA HMGCS1 Sponges miR-4521 to Aggravate Diabetes-Induced Vascular Endothelial Dysfunction Through Upregulating ARG1

Project description:Type 2 diabetes is recognized as one of the primary contributors to cardiovascular diseases, with vascular endothelial dysfunction (VED) being a crucial mechanism underlying its development. In this study, we present the aberrant expressions of CircHMGCS1 and miR-4521 in diabetes-induced VED. Overexpression of CircHMGCS1 or silencing of miR-4521 expedited the onset of diabetes and aggravated VED. Mechanistically, CircHMGCS1 upregulated ARG1 by sequestering miR-4521, resulting in the inhibition of vascular NO secretion, enhanced adhesion molecules expression of VCAM1, ICAM1, ET-1, and increased ROS generation. Consequently, these events accelerated the impairment of vascular endothelial function. These findings underscore the physiological roles of CircRNA and miRNA in cardiovascular diseases triggered by diabetes and suggest that modulating the expression of CircHMGCS1 and miR-4521 could serve as a potential strategy for preventing endothelial cell dysfunction and the development of diabetes-associated cardiovascular diseases.

2024-08-08 | GSE237295 | GEO

High-throughput sequencing of circRNA in human umbilical vein endothelial cells treated with high glucose

Project description:Atherosclerosis (AS) is a multiple factors-involved chronic inflammatory disease in the arterial wall, and is the dominant cause of cardiovascular disease (CVD). circRNAs can serve as competing endogenous RNA (ceRNA) to mRNAs and play function in multiple diseases. However, the molecular mechanisms underlying how circRNA regulates endothelial cells (ECs) abnormal transformation in AS remain unknown.Both clinical and basic studies have shown that HG-induced endothelial dysfunction is a crucial initiating factor in the development of diabetic vascular complications. In addition, studies have indicated that Ang Ⅱ is also involved in the process of atherosclerosis by inducing ECs dysfunction and regulating inflammatory responsesFor present study, therefore, we attempt to use circRNA microarray to indicate that the expression alters of circRNAs extracted from ECs treated with HG and Ang Ⅱ.

2024-09-18 | GSE206809 | GEO

Transcriptomic profiling of ZMPSTE24 knockout endothelial cells: implication of endothelial dysfunction in HGPS

Project description:Hutchinson-Gilford progeria syndrome (HGPS) is an ultrarare and fatal disease with features of premature aging and cardiovascular diseases (atherosclerosis, myocardial infarction, and stroke). The molecular basis underlying premature aging driven cardiovascular diseases remains incompletely understood. Since endothelial dysfunction is involved in the initiation and progression of cardiovascular diseases. We hypothesized that HGPS-causing progerin (a mutant form of lamin A) and farnesylated prelamin A drives endothelial dysfunction and cardiovascular disease. In our study, we performed transcriptomic profiling of ZMPSTE24-/- mouse endothelial cells, hoping to find the missing link between progeria and atherosclerosis. We observed that ZMPSTE24-/- endothelial cells have increased farnesylated prelamin A accumulation, and show nuclear structure abnormality. Analysis of RNA-seq data revealed that multiple endothelial homeostasis-related genes and pathways are altered by ZMPSTE24 deletion. Further studies are needed to characterize the biological functions of ZMPSTE24 in the pathogenesis of progeria-associated atherosclerosis.

2019-11-27 | GSE137501 | GEO

Transcription profiling of human coronary artery endothelial cells treated with ADMA at 2uM (a pathophysiological dose) and 100uM (a pharmacological dose), for 24h

Project description:Asymmetric dimethylarginine (ADMA) is a naturally occurring inhibitor of nitric oxide synthesis that accumulates in wide range of diseases associated with endothelial dysfunction and enhanced atherosclerosis. Plasma ADMA has been implicated as a major novel cardiovascular risk factor, but the mechanisms by which low concentrations of ADMA produce adverse effects on the cardiovascular system are unclear. We have treated human coronary artery endothelial cells with ADMA at 2uM (a pathophysiological dose) and 100uM (a pharmacological dose), for 24h.

2005-09-01 | E-MEXP-377 | biostudies-arrayexpress

Hyperglycemia induced microRNAs in endothelial dysfunction

Project description:Hyperglycemia is a hallmark in prediabetes and type 2 diabetes mellitus (T2DM) which increases risk of micro and macrovascular complications such as diabetic retinopathy, diabetic nephropathy (microvascular complications), and peripheral vascular disease, cerebrovascular disease and cardiovascular diseases (macrovascular complications). Endothelial cells are affected in both cases. In this study, we investigated the miRNA expression changes in HUVECs during different glucose treatment (5mM, 10mM, 25mM and 40mM glucose) at various time intervals (6, 12, 24 and 48hrs). The results of miRNA microarray showed there is a correlation between hyperglycemia induced endothelial dysfunction and miRNA expression. In silico prediction showed that the following pathways: Regulation of actin cytoskeleton, PI3K-Akt signaling pathway, Apoptosis, Neurotrophin signaling pathway, and Insulin signaling pathway, were dysregulated during hyperglycemia. Majority of the pathways are related to apoptosis. 10 miRNAs (miR-26a-5p, -26b-5p, 29b-3p, 29c-3p, 125b-1-3p, -130b-3p, - 140-5p, -221-3p, -192-5p, and -320a,) showed increased expression with increasing concentration of glucose treatment. miR-26a-5p, -29b-3p, - 140-5p, -221-3p, and -192-5p are involves in endothelial apoptosis. Our study revealed miRNAs (miR-29b-3p and – 192-5p) with known mRNA targets (BCL2 and MCL1) showed expression pattern inversely correlating with their respective target mRNAs. Therefore these miRNAs could involve in the endothelial dysfunction due to hyperglycemia.

2016-05-23 | GSE74296 | GEO

Time-dependent specific molecular signatures of inflammation and remodelling are associated with Trimethylamine-N-oxide (TMAO)-induced endothelial cell dysfunction

Project description:Cardiovascular diseases (CVDs) are leading causes of death worldwide. Endothelial dysfunction is a critical initiating factor contributing to CVDs, which progression involves the gut microbiome-derived metabolite Trimethylamine N-oxide (TMAO). Here, we aim to clarify the time-dependent pathways by which TMAO mediates endothelial dysfunction.

2023-11-23 | GSE235204 | GEO

Endothelial Overexpression protects Metabolic Homeostasis and the Development of Obesity and cardiovascular disease

Project description:Introduction: Obesity is a major risk factor associated with multiple pathological conditions including diabetes and cardiovascular disease. Endothelial dysfunction is an early predictor of obesity. However, little is known regarding how early endothelial changes trigger obesity. In the present work we report a novel endothelial-mediated mechanism essential for regulation of metabolic homeostasis, driven by c-Myc. Methods: We used conditional overexpression (EC-Myc OE) mouse models to investigate the role of endothelial-specific c-Myc in metabolic homeostasis during high-fat diet exposure. Body weight, metabolic parameters and cardiovascular function were collected over time and tissue samples collected at endpoint for biochemical, pathology and RNA-sequencing analysis. Results: In the present study we demonstrate that Overexpression of endothelial c-Myc attenuated diet-induced obesity and visceral fat accumulation and prevented the development of glucose tolerance and cardiac dysfunction. Transcriptome analysis of skeletal muscle suggests that the protective effects promoted by endothelial c-Myc overexpression are associated with the expression of genes known to increase weight loss, energy expenditure and glucose tolerance. Discussion: Our results show a novel important role for endothelial c-Myc in regulating metabolic homeostasis and suggests its potential targeting in preventing obesity and associated complications such as diabetes type-2 and cardiovascular dysfunction.

2024-05-31 | GSE267493 | GEO

RNAseq of Human Umbilical Vein Endothelial Cells treated with Insulin in the presence or absence of TGF-beta kinase inhibitor SB431542 for 90 minute.

Project description:Endothelial cells play many important role during development and development of diseases. Endothelial dysfunction which is commonly seen in diabetes patients is thought to be one of the first step that leads to adverse events such as retinopathy, nephropathy, and atherosclerosis. To examine to which extent TGF-beta signaling contributes to insulin-induced transcriptional responses we performed this RNAseq on Human umbilical vein endothelial cells.

2019-01-15 | E-MTAB-6841 | biostudies-arrayexpress

Transcriptomic profiling of differentially expressed mRNA, lncRNA and circRNA in atorvastatin-treated human endothelial cells

Project description:Statins are competitive inhibitors of (3-hydroxy-3-methylglutaryl coenzyme A) HMG-CoA reductase. The primary mechanism of statins is the lowering of serum cholesterol through inhibiting hepatic cholesterol biosynthesis. Statins exert pleiotropic vasoprotective and atheroprotective effects in the vasculature, with its mechanism of action being incompletely understood.To depict the statin-regulated mRNA,long non-coding RNA (lncRNA) and circular RNA (circRNA) in human endothelial cells, we performed transcriptomic profiling of human umbilical vein endothelial cells (HUVECs) with atorvastatin treatment.Differentially expressed mRNA, lncRNA and circRNA may represent novel therapeutic targets against cardiovascular diseases.

2023-05-31 | GSE176531 | GEO

A miR-494 dependent feedback loop regulates ER stress (ANAN-376 Project)

Project description:Defects in stress responses are important contributors in many chronic conditions including cancer, cardiovascular disease, diabetes, and obesity-driven pathologies like non-alcoholic steatohepatitis (NASH). Specifically, endoplasmic reticulum (ER) stress is linked with these pathologies and control of ER stress can ameliorate tissue damage. MicroRNAs have a critical role in regulating diverse stress responses including ER stress. Here we show that miR-494-3p plays a functional role during ER stress. ER stress inducers (tunicamycin and thapsigargin) robustly increase the expression of miR-494 in vitro in an ATF6 dependent manner. Surprisingly, miR-494 pretreatment dampens the induction and magnitude of ER stress in response to tunicamycin in endothelial cells. Conversely, inhibition of miR-494 increases ER stress de novo and amplifies the effects of ER stress inducers. Using Mass Spectrometry (TMT-MS) we identified many proteins that are downregulated by both tunicamycin and miR-494 in cultured human umbilical vein endothelial cells (HUVECs). Among these, we found 6 transcripts which harbor a putative miR-494 binding site. Our data indicates that ER stress driven miR-494 may act in a feedback inhibitory loop to dampen downstream ER stress signaling. We propose that RNA-based approaches targeting miR-494 or its targets may be attractive candidates for inhibiting ER stress dependent pathologies in human disease.

2021-09-09 | PXD019992 | Pride

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