AngII induced responses from non-myocytes in the heart
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE185756 | GEO | 2022/02/08
REPOSITORIES: GEO
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Project description:AngII infusion in mouse is a classic model of cardiac hypertrophy. Here we aimed to understand the role of neutrophils in the myocardium.
2022-02-08 | GSE186468 | GEO
Project description:AngII induced responses from non-myocytes in the heart
| PRJNA770673 | ENA
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
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 | GSE606 | GEO
Project description:Pregnancy-associated hypertensive (PAH) mice were maintained by mating females carrying the human angiotensinogen (hAGT) gene with males expressing the human renin (hRN) gene, as previously described (Takimoto E., et al., Science, 1996). Angiotensin II (AngII) has critical roles in regulation of blood pressure. In late pregnancy of PAH mice, increased AngII causes acute and severe hypertension with proteinuria. Furthermore, PAH mice show cardiac hypertrophy, fibrosis and apoptosis. It is known that AngII downregulates mRNA of alpha 1a-adrenergic receptor (Adra1a) in neonatal rat cardiac myocytes (Li H.T., et al., Circ. Res., 1997). Interestingly, we found that Adra1a knock out PAH (PAH/aKO) mice display more severe phenotype of cardiac hypertrophy in comparison to PAH mice. In this study, to understand the molecular basis of cardiac hypertrophy via regulation of Adra1a expression with AngII in PAH mice, we performed a comprehensive analysis of gene expression changes in cardiac remodeling of PAH and PAH/aKO mice using the next-generation RNA sequencing (RNA-seq).
2023-01-27 | GSE140948 | GEO
Project description:Aims: Pathological cardiac hypertrophy induced by activation of the renin–angiotensin–aldosterone system (RAAS) is one of the leading causes of heart failure. However, in current clinical practice, the strategy for targeting the RAAS is not sufficient to reverse hypertrophy. Here, we investigated the effect of prostaglandin E1 (PGE1) on angiotensin II (AngII)-induced cardiac hypertrophy and potential molecular mechanisms underlying the effect. Methods and Results: Adult male C57 mice were continuously infused with AngII or saline and treated daily with PGE1 or vehicle for two weeks. Neonatal rat cardiomyocytes were cultured to detect AngII-induced hypertrophic responses. We found that PGE1 ameliorated AngII-induced cardiac hypertrophy both in vivo and in vitro. The RNA sequencing (RNA-seq) and expression pattern analysis results suggest that Netrin-1 (Ntn1) is the specific target gene of PGE1. The protective effect of PGE1 was eliminated after knockdown of Ntn1. Moreover, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that the PGE1-mediated signaling pathway changes are associated with the mitogen-activated protein kinase (MAPK) pathway. PGE1 suppressed AngII-induced activation of the MAPK signaling pathway, and such an effect was attenuated by Ntn1 knockdown. Blockade of MAPK signaling rescued the phenotype of cardiomyocytes caused by Ntn1 knockdown, indicating that MAPK signaling may act as the downstream effector of Ntn1. Furthermore, inhibition of the E-prostanoid (EP)3 receptor, as opposed to the EP1, EP2, or EP4 receptor, in cardiomyocytes reversed the effect of PGE1, and activation of EP3 by sulprostone, a specific agonist, mimicked the effect of PGE1. Conclusion: In conclusion, PGE1 ameliorates AngII-induced cardiac hypertrophy through activation of the EP3 receptor and upregulation of Ntn1, which inhibits the downstream MAPK signaling pathway. Thus, targeting EP3, as well as the Ntn1–MAPK axis, may represent a novel approach for treating pathological cardiac hypertrophy.
2022-06-01 | GSE168350 | GEO
Project description:Obesity-induced secretory disorder of adipose tissue-derived factors is important for cardiac damage. However, whether platelet-derived growth factor-D (PDGF-D), a newly identified adipokine, regulates cardiac remodeling in Angiotensin II (AngII)-infused obese mice is unclear. Here, we found obesity induced PDGF-D expression in adipose tissue, as well as more severe cardiac remodeling compared to control lean mice after AngII infusion. Adipocyte-specific PDGF-D knockout attenuated hypertensive cardiac remodeling in obese mice. Consistently, adipocyte-specific PDGF-D overexpression transgenic mice (PA-Tg) showed exacerbated cardiac remodeling after AngII infusion without high-fat diet treatment. Mechanistic studies indicated that AngII-stimulated macrophages produce urokinase plasminogen activator (uPA) that activates PDGF-D by splicing full-length PDGF-D into the active PDGF-DD. Moreover, bone marrow specific uPA knockdown decreased active PDGF-DD level in the heart and improved cardiac remodeling in HFD hypertensive mice. Together, our data provide for the first time a new interaction pattern between macrophage and adipocyte, that macrophage-derived uPA activates adipocyte-secreted PDGF-D, which finally accelerates AngII-induced cardiac remodeling in obese mice.
2021-05-27 | GSE175572 | GEO
Project description:Background: We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy and promotes physiological hypertrophy in an aortic banding model. To identify transcriptional pathways regulated by CHF1/Hey2 in hypertrophy, we cultured primary neonatal mouse cardiac myocytes from wild type and transgenic mice overexpressing CHF1/Hey2 and treated them with serum, a potent hypertrophic stimulus. We determined transcriptional profiles by hybridization to Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays. We identified important biological processes regulated by CHF1/Hey2 by Gene Set Analysis using Biological Process Gene Sets from the Gene Ontology Consortium. Results: We found that overexpression of CHF1/Hey2 suppresses gene sets involved in water transport, regulation of adenylate cyclase activity, embryonic eye morphogenesis, gut development and fluid transport after serum stimulation. Genes involved in protein dephosphorylation, in contrast, demonstrate increased expression in myocytes overexpressing CHF1/Hey2, and this increase is independent of serum treatment. Genes overexpressed prior to serum treatment are involved in regulation of transcription factor activity, protein export from the nucleus, and steroid hormone receptor signaling. Genes overexpressed after serum treatment are involved in autophagy, apoptosis and mitochondrial biogenesis. Conclusions: CHF1/Hey2 suppresses fluid transport, activation of adenylate cyclase activity, promotes phosphatase activity, autophagy and regulates other important biological processes likely relevant to hypertrophy. Transgenic Mice and Neonatal Mouse Myocyte Culture: WT no serum, 5; WT with serum, 7; TG no serum, 6; TG with serum, 7.
2010-04-08 | E-GEOD-14288 | biostudies-arrayexpress
Project description:In order to study the capacity of the myocardium to recover from a stress causing several features of heart failure with preserved ejection fraction, C57Bl6/J male and female mice received or not for 28 days an angiotensin II (AngII; 1,5 mg/kg/day) continuous infusion in combination with a high fat diet (HFD). Half of the animals were then euthanized. The remaining ones had the AngII infusion stopped and their diet normalized. In addition, voluntary exercise was initiated by introducing a running wheel in the animals cage for an additional 28 days.
2023-12-18 | GSE240171 | GEO
Project description:Background: We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy and promotes physiological hypertrophy in an aortic banding model. To identify transcriptional pathways regulated by CHF1/Hey2 in hypertrophy, we cultured primary neonatal mouse cardiac myocytes from wild type and transgenic mice overexpressing CHF1/Hey2 and treated them with serum, a potent hypertrophic stimulus. We determined transcriptional profiles by hybridization to Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays. We identified important biological processes regulated by CHF1/Hey2 by Gene Set Analysis using Biological Process Gene Sets from the Gene Ontology Consortium. Results: We found that overexpression of CHF1/Hey2 suppresses gene sets involved in water transport, regulation of adenylate cyclase activity, embryonic eye morphogenesis, gut development and fluid transport after serum stimulation. Genes involved in protein dephosphorylation, in contrast, demonstrate increased expression in myocytes overexpressing CHF1/Hey2, and this increase is independent of serum treatment. Genes overexpressed prior to serum treatment are involved in regulation of transcription factor activity, protein export from the nucleus, and steroid hormone receptor signaling. Genes overexpressed after serum treatment are involved in autophagy, apoptosis and mitochondrial biogenesis. Conclusions: CHF1/Hey2 suppresses fluid transport, activation of adenylate cyclase activity, promotes phosphatase activity, autophagy and regulates other important biological processes likely relevant to hypertrophy.
2010-01-04 | GSE14288 | GEO