Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

High-throughput RNA sequencing of basilar artery smooth muscle cells in wild type and high-salt diet induced hypertension rats

ABSTRACT: High-throughput RNA sequencing of basilar artery smooth muscle cells in wild type and high-salt diet induced hypertension rats

PROVIDER: PRJNA622585 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11467777_1.fastq.gz	Fastqsanger.gz
	SRR11467777_2.fastq.gz	Fastqsanger.gz
	SRR11467778_1.fastq.gz	Fastqsanger.gz
	SRR11467778_2.fastq.gz	Fastqsanger.gz
	SRR11467779_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

High-throughput RNA sequencing of basilar artery smooth muscle cells in wild type and high-salt diet induced hypertension rats

Project description:We utilized high-throughput sequencing and subsequent signaling pathway analyses to find 2 fold change or greater upregulated expression of 230 transcripts and downregulated expression of 165 transcripts in basilar artery smooth muscle cells derived from rats fed a high-salt diet compared with those from control rats.

2020-04-02 | GSE147945 | GEO

Microarray-based gene expression of rabbit basilar artery smooth muscle cells exposed to hemodynamic insult

2016-06-30 | GSE61212 | GEO

Microarray-based gene expression of rabbit basilar artery smooth muscle cells exposed to hemodynamic insult

Project description:High-flow causes the remodeling of arteries, in which smooth muscle cells play an important role. To know the profile of smooth muscle gene expression under high-flow conditions in vivo, flow of rabbit basilar artery was increased by ligation of both common carotid arteries. Microarrays were performed to profile the gene expression of smooth muscle cells isolated from rabbit basilar artery. Expression profiles indicate 43603 differentially expressed genes in smooth muscle cells exposed to high-flow insult compared with the sham control, of which 1470 genes were upregulated and 780 genes downregulated using 2 fold-changes and P<0.05 as a cut-off. Bilateral common carotid arteries of female New Zealand White rabbits were ligated to increase vascular flow.The control group was performed the same procedure to expose the CCAs without ligation. Rabbits were euthanized at day 5 after ligation or exposure of bilateral CCAs in both groups (n=3 for each group). The rabbits used and all procedures in this study were approved by the local Institutional Animal Care and Use Committee. Smooth muscle cells were isolated. After euthanization of rabbits, the whole basilar arteries were removed. The arteries were cleaned in PBS buffer,cannulated and perfused at a constant flow with a cocktail which contains PBS and 0.4 mg/ml elastase (Sigma) and 1 mg/ml collagenase (type 1A, Sigma). After an incubation time of 45 min, the tissue left was removed and stored in PBS. SMCs were released from the artery by trituration. Then Total RNA was extracted and gene chip tests were performed.

2016-06-30 | E-GEOD-61212 | biostudies-arrayexpress

Intermittent short-duration reoxygenation protects against simulated high altitude-induced pulmonary hypertension in rats

Project description:High-altitude pulmonary hypertension (HAPH) is a severe and progressive disease caused by chronic hypoxia and subsequent pulmonary vascular remodeling. No cure is currently available owing to an incomplete understanding about vascular remodeling. It is believed that hypoxia-induced diseases can be prevented by treating hypoxia. Thus, this study aimed to determine whether daily short-duration reoxygenation at sea level attenuates pulmonary hypertension under high-altitude hypoxia. To this end, a simulated 5,000-m hypoxia rat model was used to evaluate the effect of short-duration reoxygenation. Results show that intermittent, not continuous, short-duration reoxygenation effectively attenuates hypoxia-induced pulmonary hypertension. The mechanisms underlining the protective effects involved that intermittent, short-duration reoxygenation prevented functional and structural remodeling of pulmonary arteries and proliferation, migration, and phenotypic conversion of pulmonary artery smooth muscle cells under hypoxia. The specific genes or potential molecular pathways responsible for mediating the protective effects were also characterised by RNA sequencing.This study is novel in revealing a new potential method in preventing high-altitude pulmonary hypertension. It gives insights into the selection and optimisation of oxygen supply schemes in high-altitude areas.

2020-11-06 | GSE160926 | GEO

RNA sequencing of healthy and diseased (idiopathic pulmonary hypertension) human pulmonary artery smooth muscle cells

Project description:We performed RNA-seq to analyze gene expression in human PASMCs (Pulmonary arterial smooth muscle cells) isolated from subjects without disease and from subjects with IPAH (idiopathic pulmonary hypertension)

2020-07-15 | GSE144274 | GEO

Mesenteric artery smooth muscle cells from hypertensive rats have increased microtubule acetylation

Project description:The dynamic nature of the microtubule network is regulated in part by post-translational modifications – particularly through acetylation, which stabilizes the microtubule network. Whether post-translational modifications of the microtubule network in vascular smooth muscle cells contribute to the pathophysiology of hypertension is unknown. The aim of this study was to determine the acetylated state of the microtubule network in the mesenteric arteries of spontaneously hypertensive rats (SHR), and investigate whether sustained acetylation via treatment with a histone deacetlyase-6 (HDAC-6) inhibitor, tubacin, would affect isoprenaline-mediated vasorelaxations in normotensive and hypertensive vessels.Using Western blotting, and mass spectrometry, we show that acetylation of the microtubule network is increased in the mesenteric arteries of the SHR compared to normotensive rats. Using wire myography, we found that tubacin enhanced the β-adrenoceptor-mediated vasodilatation by isoprenaline when the endothelium was intact, but attenuated relaxations when the endothelium was denuded or nitric oxide production was inhibited. By pre-treating vessels with colchicine to disrupt the microtubule network, we were able to confirm that the effects of tubacin were microtubule-dependent. Using SICM, we examined the cell surface Young’s Modulus of smooth muscle cells, but found no difference between control, tubacin-treated, or taxol-treated cells.Acetylation of the microtubule network is elevated in mesenteric arteries from the SHR. Furthermore, this study shows that tubacin has an endothelial-dependent bimodal effect on isoprenaline-mediated vasorelaxation. These findings pave the way for evaluation of HDAC inhibitors in the treatment of hypertension in human clinical studies.

2024-02-21 | PXD045602 | Pride

Endothelial cell senescence exacerbates pulmonary hypertension by inducing juxtacrine Notch signaling in smooth muscle cells

Project description:Pulmonary arterial hypertension (PAH) is a fatal disease characterized by a progressive increase in pulmonary artery pressure caused by pathological pulmonary artery remodeling. Here, we show that endothelial cell (EC) senescence plays a negative role in pulmonary hypertension via juxtacrine interaction with smooth muscle cells (SMCs). By using EC-specific progeroid mice that we recently generated, we discovered that EC progeria deteriorated vascular remodeling in the lungs, and exacerbated pulmonary hypertension in mice exposed to chronic hypoxia. Mechanistically, senescent ECs overexpressed Notch ligands, which resulted in increased Notch signaling and activated proliferation and migration capacities in neighboring SMCs. Pharmacological inhibition of Notch signaling reduced the effects of senescent ECs on SMCs functions in vitro, and improved the worsened pulmonary hypertension in EC-specific progeroid mice in vivo. Our findings show that EC senescence is a critical disease-modifying factor in PAH and that EC-mediated Notch signaling is a pharmacotherapeutic target for the treatment of PAH, particularly in the elderly.

2023-04-30 | GSE228491 | GEO

Transcriptional profiling of basilar artery and basilar terminus intima and media in rabbits after bilateral carotid ligation

Project description:New Zealand white rabbits underwent bilateral carotid ligation to increase flow in the basilar artery (BA) or sham surgery. 24 hours post-surgery, the BA and basilar terminus (BT) were embedded for sectioning. The intima and media were separately laser-microdissected from the sections, and whole transcriptome RNA-seq was performed on each tissue in order to more thoroughly characterize potential molecular signals between endothelium and smooth muscle during flow-induced arterial remodeling.

2021-07-28 | GSE169276 | GEO

RNA sequencing of healthy and diseased (idiopathic pulmonary hypertension) human pulmonary artery smooth muscle cells

Project description:RNA sequencing of healthy and diseased (idiopathic pulmonary hypertension) human pulmonary artery smooth muscle cells

| PRJNA603286 | ENA

A Potential Diagnostic Biomarker in Pulmonary Hypertension

Project description:Right heart failure results from advanced pulmonary hypertension (PH) and has a poor prognosis. There are few available treatments for right heart failure. Pulmonary artery remodeling, including changes in pulmonary artery endothelial cells to endothelial-mesenchymal cells, and aberrant fibroblast and pulmonary artery smooth muscle cell (PASMC) proliferation, are characteristics of the pathophysiological process of PH. As a result, the clinical situation requires novel PH diagnostic and treatment targets.

2022-10-14 | GSE215341 | 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