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RNA-seq analysis of pulmonary arterial smooth muscle cells(PASMCs)stimulated with BMP9/10

ABSTRACT: RNA-seq analysis of pulmonary arterial smooth muscle cells(PASMCs)stimulated with BMP9/10

PROVIDER: PRJNA614466 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11391680.fastq.gz	Fastqsanger.gz
	SRR11391681.fastq.gz	Fastqsanger.gz
	SRR11391682.fastq.gz	Fastqsanger.gz
	SRR11391683.fastq.gz	Fastqsanger.gz
	SRR11391684.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of pulmonary arterial smooth muscle cells(PASMCs)stimulated with BMP9/10

Project description:Inactivation of BMP9/10 in mice leads to attenuated contractility of smooth muscle cells and decreased blood pressure.Treatment of de-differentiated PASMCs with BMP9/10 resulted in a strong increase of ACTA2 expression as measured by immunofluorescence and RT-PCR, indicating a switch from the de-differentiated, synthetic to a differentiated, contractile state. To further study the role of BMP9/10 in smooth muscle cells, we isolate PSAMCs and stimulate cells with or without BMP9/10 and perform the RNA-seq analysis.

2020-05-31 | GSE147376 | GEO

Murine pulmonary arterial smooth muscle cells: Wild-type vs. NOX1 deficiency (miRNA profiling)

Project description:NOX1 is a catalytic subunit of nonphagocytic NADPH oxidase, mainly localized to smooth muscle cells in the vasculature. We investigated the pathology underlying the pulmonary arterial hypertension-like phenotype demonstrated in mice deficient in the Nox1 gene (Nox1-KO). Spontaneous enlargement and hypertrophy of the right ventricle, accompanied by hypertrophy of pulmonary vessels, were demonstrated in Nox1-KO at 9-18 weeks of age. Since an increased number of ?-smooth muscle actin-positive vessels was observed in Nox1-KO, pulmonary arterial smooth muscle cells (PASMCs) were isolated and characterized by flow cytometry and TUNEL staining. In Nox1-/Y PASMC, the number of apoptotic cells was significantly reduced without any change in the expression of endothelin-1, and hypoxia-inducible factors HIF-1a and HIF-2a, factors implicated in the pathogenesis of PAH. microRNA expression profiling of mouse pulmonary arterial smooth muscle cells in wild-type and NOX1-KO was analyzed. Pulmonary arterial smooth muscle cells were harvested form 3 mice.

2014-01-22 | E-GEOD-42015 | biostudies-arrayexpress

Murine pulmonary arterial smooth muscle cells: Wild-type vs. NOX1 deficiency (mRNA profiling)

Project description:NOX1 is a catalytic subunit of nonphagocytic NADPH oxidase, mainly localized to smooth muscle cells in the vasculature. We investigated the pathology underlying the pulmonary arterial hypertension-like phenotype demonstrated in mice deficient in the Nox1 gene (Nox1-KO). Spontaneous enlargement and hypertrophy of the right ventricle, accompanied by hypertrophy of pulmonary vessels, were demonstrated in Nox1-KO at 9-18 weeks of age. Since an increased number of α-smooth muscle actin-positive vessels was observed in Nox1-KO, pulmonary arterial smooth muscle cells (PASMCs) were isolated and characterized by flow cytometry and TUNEL staining. In Nox1-/Y PASMC, the number of apoptotic cells was significantly reduced without any change in the expression of endothelin-1, and hypoxia-inducible factors HIF-1a and HIF-2a, factors implicated in the pathogenesis of PAH. Transcriptional profiling of mouse pulmonary arterial smooth muscle cells in wild-type and NOX1-KO was analyzed. Pulmonary arterial smooth muscle cells were harvested from 3 mice.

2014-01-22 | E-GEOD-42014 | biostudies-arrayexpress

Pro-BMP9 and pro-BMP10 signalling in pulmonary arterial endothelial cells

Project description:This study was designed to compare the global gene expression change induced by the circulating, prodomain bound forms of BMP9 and BMP10 (pro-BMP9 and pro-BMP10) in human pulmonary arterial endothelial cells (PAECs). This is different from many previous studies which used the growth factor domain of BMP9 and/or BMP10.

2020-03-04 | GSE134890 | GEO

Murine pulmonary arterial smooth muscle cells: Wild-type vs. NOX1 deficiency (mRNA profiling)

Project description:NOX1 is a catalytic subunit of nonphagocytic NADPH oxidase, mainly localized to smooth muscle cells in the vasculature. We investigated the pathology underlying the pulmonary arterial hypertension-like phenotype demonstrated in mice deficient in the Nox1 gene (Nox1-KO). Spontaneous enlargement and hypertrophy of the right ventricle, accompanied by hypertrophy of pulmonary vessels, were demonstrated in Nox1-KO at 9-18 weeks of age. Since an increased number of α-smooth muscle actin-positive vessels was observed in Nox1-KO, pulmonary arterial smooth muscle cells (PASMCs) were isolated and characterized by flow cytometry and TUNEL staining. In Nox1-/Y PASMC, the number of apoptotic cells was significantly reduced without any change in the expression of endothelin-1, and hypoxia-inducible factors HIF-1a and HIF-2a, factors implicated in the pathogenesis of PAH. Transcriptional profiling of mouse pulmonary arterial smooth muscle cells in wild-type and NOX1-KO was analyzed.

2014-01-22 | GSE42014 | GEO

Murine pulmonary arterial smooth muscle cells: Wild-type vs. NOX1 deficiency (miRNA profiling)

Project description:NOX1 is a catalytic subunit of nonphagocytic NADPH oxidase, mainly localized to smooth muscle cells in the vasculature. We investigated the pathology underlying the pulmonary arterial hypertension-like phenotype demonstrated in mice deficient in the Nox1 gene (Nox1-KO). Spontaneous enlargement and hypertrophy of the right ventricle, accompanied by hypertrophy of pulmonary vessels, were demonstrated in Nox1-KO at 9-18 weeks of age. Since an increased number of α-smooth muscle actin-positive vessels was observed in Nox1-KO, pulmonary arterial smooth muscle cells (PASMCs) were isolated and characterized by flow cytometry and TUNEL staining. In Nox1-/Y PASMC, the number of apoptotic cells was significantly reduced without any change in the expression of endothelin-1, and hypoxia-inducible factors HIF-1a and HIF-2a, factors implicated in the pathogenesis of PAH. microRNA expression profiling of mouse pulmonary arterial smooth muscle cells in wild-type and NOX1-KO was analyzed.

2014-01-22 | GSE42015 | GEO

Pro-BMP9 signalling in human pulmonary arterial endothelial cells after 5 hours treatment

Project description:This study was designed to investigate the global gene expression of circulating, prodomain bound form of BMP9 (pro-BMP9) in human pulmonary arterial endothelial cells (PAECs) because previous microarray experients have used the growth factor domain alone. We are interested in its signalling capacity in pulmonary vascular endothelial cells using the physiological circulating form and at physiologically circulating concentrations. Also, this study reports data 5 hours after the treatment to look at the secondary genes regulated by BMP9 signalling.

2021-08-08 | GSE118353 | 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

DNA methylation signatures of pulmonary arterial smooth muscle cells in chronic thromboembolic pulmonary hypertension

Project description:DNA methylation signatures of pulmonary arterial smooth muscle cells in chronic thromboembolic pulmonary hypertension

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Anti-proliferative effect of selexipag active metabolite MRE-269 on pulmonary arterial smooth muscle cells from patients with chronic thromboembolic pulmonary hypertension

Project description:Chronic thromboembolic pulmonary hypertension (CTEPH) is a group 4 pulmonary hypertension (PH) characterized by non-resolving thromboembolism in the central pulmonary artery and vascular occlusion in the proximal and distal pulmonary artery. Medical therapy is chosen for patients who are ineligible for pulmonary endarterectomy or balloon pulmonary angioplasty or who have symptomatic residual PH after surgery or intervention. Selexipag, an oral prostacyclin receptor agonist and potent vasodilator, was approved for CTEPH in Japan in 2021. To evaluate the pharmacological effect of selexipag on vascular occlusion in CTEPH, we examined how its active metabolite MRE-269 affects platelet-derived growth factor-stimulated pulmonary arterial smooth muscle cells (PASMCs) from CTEPH patients. MRE-269 showed a more potent anti-proliferative effect on PASMCs from CTEPH patients than on those from normal subjects. DNA-binding protein inhibitor genes ID1 and ID3 were found by RNA sequencing and real-time quantitative polymerase chain reaction to be expressed at lower levels in PASMCs from CTEPH patients than in those from normal subjects and were upregulated by MRE-269 treatment. ID1 and ID3 upregulation by MRE-269 was blocked by co-incubation with a prostacyclin receptor antagonist, and ID1 knockdown by small interfering RNA transfection attenuated the anti-proliferative effect of MRE-269. ID signaling may be involved in the anti-proliferative effect of MRE-269 on PASMCs. This is the first study to demonstrate the pharmacological effects on PASMCs from CTEPH patients of a drug approved for the treatment of CTEPH. Both the vasodilatory and the anti-proliferative effect of MRE-269 may contribute to the efficacy of selexipag in CTEPH.

2022-12-27 | GSE221511 | GEO

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