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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.

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RNA-seq analysis of pulmonary arterial smooth muscle cells (PASMCs), bronchial smooth muscle cells(BSMCs) and venous SMCs in the lung

Project description:Information about the differences among arterial, venous, and bronchial smooth muscle cells (SMCs) in the lung is particularly valuable, as these distinct SMC populations are differentially affected in pulmonary diseases such as asthma, chronic obstructive pulmonary disease (COPD), and pulmonary arterial hypertension (PAH). To directly compare these SMC subtypes, we employed a combination of genetic tools and fluorescence-activated cell sorting (FACS) isolation strategies.We generated an ASMC-effector mouse line by combining Cspg4/Acta2 intersectional genetics, enabling specific targeting of vascular SMCs, including pulmonary arterial SMCs (PASMCs). To target non-vascular SMCs, including bronchial SMCs (BSMCs), we generated the NVSMC-effector mouse line using Chrm2/Acta2 intersectional genetics. As no driver specific to venous vascular SMCs (VVSMCs) is currently available, we used the transgenic reporter line [Tg(Acta2-GFP)], which labels all pulmonary SMCs, including venous SMCs.

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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

RNA-seq analysis of pulmonary arterial smooth muscle cells (PASMCs) and bronchial smooth muscle cells (BSMCs) after pulmonary arterial hypertension (PAH) treatment

Project description:RNA-seq analysis of pulmonary arterial smooth muscle cells (PASMCs) and bronchial smooth muscle cells (BSMCs) after pulmonary arterial hypertension (PAH) treatment

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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

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

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

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2026-04-11 | GSE301479 | GEO

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