Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

AngII induced responses from non-myocytes in the heart

ABSTRACT: AngII induced responses from non-myocytes in the heart

PROVIDER: PRJNA770673 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16301630_1.fastq.gz	Fastqsanger.gz
	SRR16301630_2.fastq.gz	Fastqsanger.gz
	SRR16301631_1.fastq.gz	Fastqsanger.gz
	SRR16301631_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

AngII induced responses from non-myocytes in the heart

Project description:AngII infusion in mouse is a classic model of cardiac hypertrophy. Here we aimed to understand how non-myocytes in the myocardium respond to AngII stimulation.

2022-02-08 | GSE185756 | GEO

Single-cell analysis of non-myocytes during heart regeneration reveals sequential coordinated responses from distinct cell populations.

Project description:Single-cell analysis of non-myocytes during heart regeneration reveals sequential coordinated responses from distinct cell populations.

| PRJNA608906 | ENA

Mitochondrial functional aberrations in a mouse model of non-ischemic heart failure

Project description:We characterized the metabolic and cardiac mitochondrial function in a mouse model of non-ischemic HF. Inhibition of nitric oxide synthesis and hypertension, which often present together, are two important risk factors in human non-ischemic HF. Compared with L-NAME L-NG-Nitroarginine methyl ester (L-NAME), an inhibitor of nitric oxide synthesis or Angiotensin II (AngII), a hypertensive agent treatment alone, L-NAME+AngII induced the most severe HF phenotype characterized by edema, hypertrophy, fibrosis, increased blood pressure and reduced ejection fractions. L-NAME+AngII treated mice had robust deterioration of cardiac mitochondrial function we observed. Microarray analyses revealed majority of the gene changes attributed to the combination of L-NAME+AngII. Pathway analyses indicated significant changes in metabolic pathways such as mitochondrial oxidative phosphorylation, fatty acid metabolism and tricarboxylic acid pathways etc.in L-NAME+AngII hearts. We conclude that combination of L-NAME+AngII exacerbates cardiac contractile and mitochondrial functional de-regulation compared with L-NAME and AngII alone, resulting in non-ischemic HF. This model of heart failure may be highly valuable in studying mechanisms and treatments for non-ischemic heart failure. Twelve week-old C57BL6 male mice were randomly assigned to 4 groups: 1. Control, 2. L-NAME treatment, 3. AngII treatment, 4. L-NAME+AngII treatment.L-NAME (0.3 mg/ml with 1% NaCl) was administered in drinking water. AngII (0.7 mg/kg/day) was administered via subcutaneous micro-osmotic pumps. L-NAME and AngII were administered to mice for 5 weeks and 4 weeks in combination to induce HF or alone to study the effects of the individual agents.

2016-01-19 | E-GEOD-72132 | biostudies-arrayexpress

Mitochondrial functional aberrations in a mouse model of non-ischemic heart failure

2016-01-19 | GSE72132 | GEO

Single-cell analysis of non-myocytes during heart regeneration reveals sequential coordinated responses from distinct cell populations [scRNA-seq]

Project description:Single-cell analysis of non-myocytes during heart regeneration reveals sequential coordinated responses from distinct cell populations [scRNA-seq]

| PRJNA608912 | ENA

Single-cell analysis of non-myocytes during heart regeneration reveals sequential coordinated responses from distinct cell populations [bulk RNA-seq]

Project description:Single-cell analysis of non-myocytes during heart regeneration reveals sequential coordinated responses from distinct cell populations [bulk RNA-seq]

| PRJNA608913 | ENA

Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure (rat sample)

Project description:Non-canonical Wnt signaling activated by Wnt5a and Wnt11 is required for the development of second heart field cardiac progenitor cells in mice. However, the pathophysiological role of non-canonical Wnt signaling in the adult heart has not been fully elucidated. Here we show that cardiomyocyte-specific Wnt5a knockout mice exhibit improved systolic function and reduced expression of mechanosensitive genes including Nppb compared to control mice when subjected to pressure overload. In cultured cardiac myocytes, Wnt5a knockdown reduces the upregulation of Nppb gene expression and YAP nuclear translocation induced by cyclic cell stretch. Wnt5a knockdown-induced Nppb downregulation in response to cell stretch is rescued by inhibition of Hippo pathway, and the rescue effect of Hippo inhibition is canceled by YAP knockdown. These results collectively suggest that Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure.

2023-07-17 | GSE200666 | GEO

Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure (mouse sample)

2023-07-17 | GSE200665 | GEO

Intact ureteric buds gene expression with AngII treatment

Project description:Compare the gene expression in intact Ubs after treated with AngII vs. Media, determine the key genes related to the ub branching gene expression change pattern. Two condition experiments, media and AngII. Biological replicate. Two for media samples, two for AngII treatment samples.

2010-11-01 | E-GEOD-24932 | biostudies-arrayexpress

Control vs. AngII Infusion

Project description:The genetic background of mice used in this study is mainly C57BL/6J with a small contribution from 129/Sv and DBA/2J strains. Male littermates were received continuous administration of AngII for 7 days at 0.9ug/hour. On day 7 of AngII infusion, the blood pressure of infused mice was (mmHg, mean ± SD) 156 ± 1, while the control littermates remained normotensive (106 ± 9). Keywords: other

2003-10-20 | E-GEOD-606 | biostudies-arrayexpress

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