Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA293926 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To investigate the roles of miRNAs in sepsis-induced cardiac dysfunction, we performed microarray analysis to examine microRNA profiles in mice hearts exposed to LPS versus Saline control.
2018-08-08 | GSE72380 | GEO
Project description:To identify the microRNA (miR) profile in the hearts of mice that were treated with lipopolysaccharide (LPS) and compare this profile with respective profiles that have been published in studies with mice that underwent pressure overload heart failure, 8 mouse samples were hybridized to Sanger 14 Multi-Species miR microarrays. As a result, we observed that particular cardiac miRs that are modulated during pressure overload heart failure are not affected significantly by treatment with LPS Total RNA from pieces of hearts obtained from 8 C57BL/6 mice that were treated either with saline (4 mice) or with lipopolysacharide (4 mice).
2011-06-14 | E-GEOD-29914 | biostudies-arrayexpress
Project description:To identify the microRNA (miR) profile in the hearts of mice that were treated with lipopolysaccharide (LPS) and compare this profile with respective profiles that have been published in studies with mice that underwent pressure overload heart failure, 8 mouse samples were hybridized to Sanger 14 Multi-Species miR microarrays. As a result, we observed that particular cardiac miRs that are modulated during pressure overload heart failure are not affected significantly by treatment with LPS
2011-06-14 | GSE29914 | GEO
Project description:To identify the messenger RNA (mRNA) profile in the hearts of mice that were treated with lipopolysaccharide (LPS) and identify potential changes in the expression of genes that may account for inhibition of cardiac Ppara that has been observed in LPS-treated mice, 8 mouse samples were analyzed with whole genome microarrays.
2014-12-06 | GSE63920 | GEO
Project description:To investigate the mechanism of TRPC1 or TRPC6 on the regulation of endotoxemic cardiac dysfunction, we established Trpc1-/- and Trpc6-/- mice. LPS-challenged endotoxemic mouse model was built, and the gene expression profile was analyzed using data obtained from RNA-seq of WT, LPS-challenged WT, LPS-challenged Trpc1-/-, and LPS-challenged Trpc6-/- mice hearts.
2022-11-06 | GSE217156 | GEO
Project description:C57BL6/J mice were treated with anti-PD-1 for 2 or 4 weeks, or with isotype control antibody. In echocardiography, cardiac dysfunction was seen both after 2 and 4 weeks, with decreased ejection fraction and left ventricular dilation. Bulk RNA sequencing of the hearts after treatment was performed to identify the mechanisms of anti-PD-1-induced cardiac dysfunction.
2022-12-03 | E-MTAB-12388 | biostudies-arrayexpress
Project description:Cardiac-specific PPARalpha transgenic (Tg-PPARalpha) mice show mild cardiac hypertrophy and systolic dysfunction. The failing heart phenotypes observed in Tg-PPARalpha are exacerbated by crossing with cardiac-specific Sirt1 transgenic (Tg-Sirt1) mice, whereas Tg-Sirt1 mice themselves do not show any cardiac hypertrophy or systolic dysfunction. To investigate the mechanism leading to the failing heart phenotypes in TgPPARalpha/Tg-Sirt1 bigenic mice, microarray analyses were performed. The microarray analyses revealed that many ERR target genes were downregulated in Tg-PPARalpha and in Tg-Sirt1, and they were further downregulated in the Tg-PPARalpha/Tg-Sirt1 bigenic mice. Four groups of cardiac-specific transgenic mice were used for the study, i.e., control, PPARalpha, Sirt1 and PPARalpha/Sirt1. Hearts were dissected after 10-11 weeks of male FVB background transgenic mice. Total RNA was prepared from the hearts to conduct the microarray analyses.
2011-12-01 | E-GEOD-33101 | biostudies-arrayexpress
Project description:Presence of ectopic lipid droplets (LDs) in cardiac muscle is associated to lipotoxicity and tissue dysfunction. However, presence of LDs in heart is also observed in physiological conditions, such as at times when cellular energy needs and energy production from mitochondria fatty acid (FA) ?-oxidation are high (fasting). This suggests that development of tissue lipotoxicity and dysfunction is not simply due to the presence of LDs in cardiac muscle but due at least in part to alterations in LD function. To examine the function of cardiac LDs, we obtained transgenic mice with heart-specific plin5 over-expression (MHC-plin5), a member of the perilipin protein family. Hearts from MHC-plin5 mice expressed at least 4-fold higher levels of plin5 and exhibit a 3.5- fold increase in triglyceride content versus non-transgenic littermate. Chronic cardiac excess of LDs was found to result in mild heart dysfunction with decreased expression of PPAR? target genes, decreased mitochondria function and left ventricular concentric hypertrophia. Lack of more severe heart function complications may have been prevented by a strong increased expression of oxidative induced genes via NF-E2-related factor 2 anti-oxidative pathway. Perilipin 5 regulates the formation and stabilization of cardiac LDs, and promotes cardiac steatosis without major heart function impairment. Hearts from Four MCH-Plin5 mice and four control mice at the age of 12 weeks were harvested
2013-02-09 | E-GEOD-44192 | biostudies-arrayexpress
Project description:To identify a novel target for the treatment of heart failure, we examined gene expression in the failing heart. Among the genes analyzed, 12/15 lipoxygenase (12/15-LOX) was markedly up-regulated in heart failure. To determine whether increased expression of 12/15-LOX causes heart failure, we established transgenic mice that overexpressed 12/15-LOX in cardiomyocytes. Echocardiography showed that 12/15-LOX transgenic mice developed systolic dysfunction. Cardiac fibrosis increased in 12/15-LOX transgenic mice with advancing age, and was associated with the infiltration of macrophages. Consistent with these observations, cardiac expression of monocyte chemoattractant protein-1 (Mcp-1) was up-regulated in 12/15-LOX transgenic mice compared with wild-type mice. Treatment with 12-hydroxy-eicosatetraenotic acid, a major metabolite of 12/15-LOX, increased MCP-1 expression in cardiac fibroblasts and endothelial cells, but not in cardiomyocytes. Inhibition of Mcp-1 reduced the infiltration of macrophages into the myocardium and prevented both systolic dysfunction and cardiac fibrosis in 12/15-LOX transgenic mice. Likewise, disruption of 12/15-LOX significantly reduced cardiac Mcp-1 expression and macrophage infiltration, thereby improving systolic dysfunction induced by chronic pressure overload. Our results suggest that cardiac 12/15-LOX is involved in the development of heart failure and that inhibition of 12/15-LOX could be a novel treatment for this condition. Heart failure is still one of the leading causes of death worldwide. Therefore, it is important to elucidate the underlying mechanisms of heart failure and develop more effective treatments for this condition. To clarify the molecular mechanisms of heart failure, we performed microarray analysis using cardiac tissue samples obtained from a hypertensive heart failure model (Dahl salt-sensitive rats). ~300 genes showed significant changes of expression in the failing hearts compared with control hearts. Among the genes analyzed, 12/15-lipoxygenase (12/15-LOX) was most markedly up-regulated in failing hearts compared with control hearts .
2009-06-06 | E-GEOD-16199 | biostudies-arrayexpress
Project description:Lipid (Plasmalogen) levels can be modulated via a dietary supplement called alkylglycerols (AG) which has demonstrated benefits in some disease settings. However, its therapeutic potential in cardiomyopathy remains unknown. This study explored an optimized AG supplement in restoring plasmalogen levels and attenuate cardiac dysfunction/pathology. Here, we placed a cardiac-specific transgenic cardiomyopathy mouse model, with cardiac function and molecular landscape assessed. AG supplementation increased total plasmalogens in DCM hearts and attenuated lung congestion of both sexes, but only prevented cardiac dysfunction in males. This was associated with cardiac and renal enlargement, a more favorable pro-cardiac gene expression profile, and a trend for lower cardiac fibrosis. By lipidomics, specific d18:1 ceramide species associated with cardiac pathology were lower in the DCM hearts from mice on the AG diet, and tetra-linoleoyl cardiolipin, a lipid crucial for mitochondria function was restored with AG supplementation. Proteomic analysis of hearts from male DCM mice receiving AG supplementation revealed enrichment in mitochondrial protein network, as well as upregulation of extracellular matrix binding proteins associated with cardiac regeneration. Here we highlight that AG supplementation restored plasmalogens in DCM hearts, but showed greater therapeutic potential in males than females
2024-08-08 | MSV000095560 | MassIVE