Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Novel Roles of Nrf3-Trim5 Axis in Vascular Smooth Muscle Cell Dysfunctions and Neointimal Hyperplasia

ABSTRACT: Novel Roles of Nrf3-Trim5 Axis in Vascular Smooth Muscle Cell Dysfunctions and Neointimal Hyperplasia

PROVIDER: PRJNA1186078 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Novel Roles of Nrf3-Trim5 Axis in Vascular Smooth Muscle Cell Dysfunctions and Neointimal Hyperplasia

Project description:Neointimal hyperplasia (NIH), driven by vascular smooth muscle cell (VSMC) dysfunction, is a key factor in vascular diseases like atherosclerosis and restenosis. While Nrf3 is known to regulate VSMC differentiation, its role in NIH remains unclear. Using transcriptomic data, Nrf3 knockout mice (global), we assessed Nrf3’s impact on VSMC function and NIH. We identified Trim5, a gene linked to coronary artery disease, as a downstream target of Nrf3, which promotes autophagy in VSMCs and injured arteries, enhancing VSMC dysfunction and NIH. Nrf3 overexpression increased VSMC proliferation, migration, and inflammation, while deletion or knockdown had the opposite effects. Nrf3-/- and Nrf3ΔSMC mice showed reduced VSMC accumulation and attenuated NIH after vascular injury. These findings highlight Nrf3 as a novel modulator of VSMC dysfunction and injury-induced NIH, with potential for therapeutic targeting of the Nrf3-Trim5 axis to treat NIH-related vascular diseases.

2024-12-02 | GSE281869 | GEO

Inhibition of PARP 1 Protects Against Hyperglycemic-induced Neointimal Hyperplasia by Upregulating TFPI-2 Activity

Project description:To investigate the function and potential mechanism of PARP-1 poly(ADP-ribose) polymerase 1 (PARP1) in diabetic neointimal hyperplasia. Type 1 diabetes mellitus was induced using streptozotocin (STZ) in wild-type mice and PARP1-/- mice, and ligation of the left carotid artery was performed to induce neointimal hyperplasia. Ligated carotid arteries from diabetic mice developed more extensive neointimal hyperplasia and showed greater proliferation and migration than arteries from nondiabetic mice. The augmented remodeling response was absent in diabetic mice deficient in PARP1. PARP1 deficiency reduces diabetic neointimal hyperplasia by upregulating tissue factor pathway inhibitor (TFPI)-2, which acted as a suppressor of vascular smooth muscle cell (VSMCs) proliferation and migration. The underlying mechanisms involve PARP1 that acts as a negative transcription factor by enhancing TFPI-2 promoter DNA methylation. Our studies demonstrated for the first time that Inhibition of PARP1 alleviates neointimal hyperplasia in diabetes by up-regulating TFPI-2 expression and blocking VSMC proliferation and migration. The development of PARP1 inhibitors might serve to limit mainly proliferative and migratory processes in restenosis-prone diabetic patients

2019-11-30 | GSE141193 | GEO

Deletion of hyaluronan synthase 3 inhibits neointimal hyperplasia

Project description:Affymetrix Mouse Gene 2.0 ST Gene Expression Microarrays were used to analyze differentially expressed genes after carotid artery ligation. The aim of this experiment was to detect genes regulated in Has3 deficient as compared to wildtype controls that might be involved in neointimal hyperplasia. Neointimal hyperplasia was induced in female Has3 deficient mice and wildtype controls by ligation of the left common carotid artery. Carotid transcriptome was analyzed 5 days after surgery in ligated and non-ligated carotid arteries.

2015-11-24 | E-GEOD-70410 | biostudies-arrayexpress

Fractalkine Antibody Attenuates Venous Neointimal Hyperplasia of Arteriovenous Fistula in Mice model

Project description:Fractalkine Antibody Attenuates Venous Neointimal Hyperplasia of Arteriovenous Fistula in Mice model

2021-09-15 | GSE161555 | GEO

Single-cell Transcriptome Analysis Reveals the Dynamic Populations of Vascular Cells in Neointimal Hyperplasia

Project description:Neointimal hyperplasia (NIH) are the major causes of re-stenosis in coronary intervention. Fibroblasts, vascular smooth muscle cells and endothelial cells are the main disease-causing cells in NIH. However, Yet how these cells contribute to the pathophysiology of NIH remains elusive. This study was aimed at gaining new insights into the heterogeneity of these cells by using single-cell RNA sequencing and up-to-date analytical method.

2023-11-14 | GSE244246 | GEO

Deletion of hyaluronan synthase 3 inhibits neointimal hyperplasia

2015-11-24 | GSE70410 | GEO

1α,25-Dihydroxyvitamin D3 encapsulated in Nanoparticles Prevents Venous Neointimal Hyperplasia and Stenosis in Porcine Arteriovenous Fistulas

Project description:1α,25-Dihydroxyvitamin D3 encapsulated in Nanoparticles Prevents Venous Neointimal Hyperplasia and Stenosis in Porcine Arteriovenous Fistulas

2021-04-07 | GSE161554 | GEO

Umbilical Cord Mesenchymal Stem Cells Derived Exosomal microRNA-148a-3p Inhibits Neointimal Hyperplasia by Targeting Serpine1

Project description:Restenosis is an inescapable problem when patients underwent percutaneous transluminal angioplasty because of intimal hyperplasia. Human umbilical cord mesenchymal stem cells derived exosomes (HucMSC-Exo) have been proved to promote reendothelialization to restrain the process of intimal hyperplasia. However, aberrant vascular smooth muscle cell (VSMC) proliferation, migration and dedifferentiation play more important roles in intimal hyperplasia, the effects and mechanisms of HucMSC-Exo upon VSMC are elusive

2022-12-30 | GSE188896 | GEO

Fractalkine Antibody Attenuates Venous Neointimal Hyperplasia of Arteriovenous Fistula in Mice model

Project description:Fractalkine Antibody Attenuates Venous Neointimal Hyperplasia of Arteriovenous Fistula in Mice model

| PRJNA678708 | ENA

Gene expression profile of PTPN14 silence with PDGF-BB stimulation in HA-VSMCs

Project description:The moderate response of smooth muscle cells is beneficial to the repair of vascular injury, while the continuous exposure of intravascular growth factors, and other stimulating factors will cause the dysfunction of smooth muscle cells, leading to the pathological remodeling of blood vessels, which is called neointimal hyperplasia. The aim of this study is to investigate the biological function of PTPN14 in vascular smooth muscle cells (VSMCs) and the mechanism of PTPN14 in regulating neointimal hyperplasia.

2024-07-17 | GSE267140 | 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