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Pharmacological inhibition of G9a ameliorates pulmonary vascular remodeling in PAH

ABSTRACT: Pharmacological inhibition of G9a ameliorates pulmonary vascular remodeling in PAH

PROVIDER: PRJNA826869 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18759003_1.fastq.gz	Fastqsanger.gz
	SRR18759003_2.fastq.gz	Fastqsanger.gz
	SRR18759004_1.fastq.gz	Fastqsanger.gz
	SRR18759004_2.fastq.gz	Fastqsanger.gz
	SRR18759005_1.fastq.gz	Fastqsanger.gz

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Pharmacological inhibition of G9a ameliorates pulmonary vascular remodeling in PAH

Project description:Background:Pulmonary arterial hypertension (PAH) is a severe condition characterized by progressive vascular remodeling of small pulmonary arteries (PAs) causing sustained elevation of PA pressure, right ventricular failure and death. Similar to cancer cells, PA smooth muscle cells (PASMCs), which play a key role in pulmonary vascular remodeling, have adopted multiple mechanisms to sustain their survival and proliferation in the presence of stress. The histone methyltransferase G9a has been shown to exert oncogenic effects and to serve as a buffer against an exaggerated transcriptional response. Therefore, we hypothesized that G9a up-regulation in PAH plays a pivotal role in pulmonary vascular remodeling by maintaining the abnormal phenotype of PAH-PASMCs. Methods: G9alevels were measured in PAs and isolated PASMCs of PAH patients and animal models. Selective G9a pharmacological inhibitors were used in human PAH-PASMCs and in rodent PAH models (i.e.Fawn-Hooded rats and Sugen/Hypoxia-exposed mice). Results: We present evidence of increased expression of G9a in PASMCs from PAH patients as well as in remodeled PAs from animal models. We found that pharmacological inhibition of G9a activity using BIX01294 and UNC0642significantly reduces the prosurvival and proproliferative potentials of cultured PAH-PASMCs. Using RNA sequencing, further exploration revealed that G9a promotes extracellular matrix production and affords protection against the negative effects of an overactive stress response. Finally, we found that therapeutic treatment with BIX01294 reduced pulmonary vascular remodeling and lowered mean PA pressure in Fawn-Hooded rats. Treatment of Sugen/hypoxia-challenged mice with BIX01294 also improved pulmonary hemodynamics and right ventricular function. Conclusions:These findings suggest that G9a inhibition may represent a new therapeutic approach in PAH.

2023-01-20 | GSE200821 | GEO

Limited systemic sclerosis patients with PAH show biomarkers of inflammation and vascular injury

Project description:Limited systemic sclerosis patients with pulmonary arterial hypertension show biomarkers of inflammation and vascular injury Forty-nine PBMC samples were obtained from 21 lSSc subjects without PAH (lSSc-noPAH), 15 lSSc subjects with PAH (lSSc-PAH), and 10 healthy controls; three subjects provided PBMCs one year later. Genome-wide gene expression was measured for each sample. Gene expression clearly distinguished lSSc samples from healthy controls, and separated lSSc-PAH from lSSc-NoPAH patients. The gene expression and cytokine profiles of lSSc-PAH patients suggest the presence of activated monocytes, and show markers of vascular injury and inflammation. Sample vs reference, total RNA isolated from peripheral blood mononuclear cells (PBMC), 21 lSSc subjects without PAH (lSSc-noPAH), 15 lSSc subjects with PAH (lSSc-PAH), and 10 healthy controls

2010-10-27 | E-GEOD-19617 | biostudies-arrayexpress

Limited systemic sclerosis patients with PAH show biomarkers of inflammation and vascular injury

2010-10-27 | GSE19617 | GEO

Transcription profiling of mouse lung from hypoxic pulmonary hypertension to SM22-tet-BMPR2delx4+ PAH

Project description:Comparison of lung from hypoxic PAH to SM22-tet-BMPR2delx4+ PAH, with three different types of control Experiment Overall Design: One chip each of five conditions, with pooled RNA on each chip to reduce individual variability

2008-06-12 | E-GEOD-2773 | biostudies-arrayexpress

Comprehensive transcriptome analysis of the heart in control, PAH and PAH/aKO mice.

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

Reversible and irreversible PAH in a rat model for MCT+Shunt-induced PAH and hemodynamic unloading.

Project description:PAH was induced by 60mg/kg MCT and an aorto-caval shunt. At different timepoints of PAH progression (day 14, 21 and 28 after MCT-injection), the left lung with PAH was hemodynamically unloading by unilateral orthotopic transplatation into a syngeneic, healthy recipient. All day 14 and 7/10 day 21 transplanted lungs showed reversal of PAH after LTx. All day 28 and 3/10 day 21 transplanted lungs showed PAH progression after LTx. Lung tissue of Reversible and Irreversible PAH and normal controls, acquired at LTx, was compared using RNA-seq.

2020-07-01 | GSE149899 | GEO

Pharmacological inhibition of the MAPK pathway ameliorates RIT1M90I-driven cardiac tissue hypertrophy.

Project description:Pharmacological inhibition of the MAPK pathway ameliorates RIT1M90I-driven cardiac tissue hypertrophy.

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Genetic and pharmacological targeting of hepatic oxalate overproduction ameliorates metabolic dysfunction-associated steatohepatitis

Project description:Genetic and pharmacological targeting of hepatic oxalate overproduction ameliorates metabolic dysfunction-associated steatohepatitis

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Single Cell RNA sequencing of the Monocytes from controls and pulmonary arterial hypertension (PAH) patients

Project description:We report the application of single cell RNA sequencing on human Peripheral Blood Mononuclear cells. The 12 samples are sequenced as biological replications (6 control and 6 patients), and pooled at the analysis stage. The library was prepared using the Chromium Single Cell 3' v2 and v3 Reagent Kit, and sample processing was under bcl2fastq2/2.20.0 and cellranger/2.2.0. We report a decreased CD14 in classical monocytes among PAH patients, with greater potential of apoptosis for CD14+ monocytes population. This study provide a reference for studying the monocytes related abonormalties in PAH and other inflammatory diseases.

2023-06-01 | GSE233189 | GEO

Genome-wide analysis of gene expression in pericytes extracted from pulmonary aterial hypertension (PAH) patients

Project description:Performed a transcriptome analysis of patient-derived donor control and PAH lung pericytes followed by functional genomics analysis. Diseased pericytes demonstrated significant enrichment of genes involved in various metabolic processes

2017-01-19 | GSE79786 | GEO

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