Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA556695 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

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

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

Transcriptional profiling of mouse aorta after deletion of BMP9 and BMP10

Project description:Aorta was isolated from ANF-Cre positive/BMP10 loxP/loxP/BMP9-/- (BMP9/10 dKO) mice. ANF-Cre negative BMP10 loxP/loxP mice were used as controls. Transcritional profiling was performed to understand the impact of BMP9/10 expression on aorta function.

2021-02-05 | GSE160026 | GEO

Transcriptional profiling of mouse aorta after deletion of BMP9 and BMP10.

Project description:Aorta was isolated from ANF-Cre positive / BMP10 loxP/loxP / BMP9-/- (BMP9/10 dKO) mice. ANF-Cre negative BMP10 loxP/loxP mice were used as controls. Transcriptional profiling was performed to understand the importance of BMP9/10 expression on aorta function.

2020-10-30 | E-MTAB-8914 | biostudies-arrayexpress

Deciphering early phosphoproteome changes in response to BMP9 and BMP10 in endothelial cells

Project description:BMP9 and BMP10 are two key regulators of vascular homeostasis. These two ligands bind with high affinity to the endothelial type I receptor ALK1 together with a type 2 receptor. Mutations in this signaling pathway have been identified in two rare cardiovascular diseases, hereditary hemorrhagic telangiectasia and pulmonary arterial hypertension. So far, only the canonical SMAD signaling pathway has been extensively studied in response to BMPs. The aim of this work was to address early phosphoproteomic changes in endothelial cells in response to short-term stimulation (30 mins) with BMP9 and BMP10 in order to identify new phosphorylated targets and signaling pathways.

2024-03-25 | PXD044952 | Pride

Pro-BMP9 and sENG monomer:BMP9 complex signalling in human pulmonary arterial endothelial cells after 1.5 hours treatment

Project description:This experiment was desinged to investigate the difference in global gene expression induced by the circulating form of BMP9, pro-BMP9, and BMP9 in complex with soluble endoglin (sENG:BMP9).

2019-09-23 | GSE119206 | GEO

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

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

| PRJNA485326 | ENA

Pro-BMP9 and sENG monomer:BMP9 complex signalling in human pulmonary arterial endothelial cells after 1.5 hours treatment

Project description:Pro-BMP9 and sENG monomer:BMP9 complex signalling in human pulmonary arterial endothelial cells after 1.5 hours treatment

| PRJNA488465 | ENA

BMP9 and BMP10 coordinate liver cellular crosstalk to maintain liver health

Project description:The liver is a largest solid organ in the body and is majorly composed of HCs, ECs, KCs, and HSCs, which spatially interact and cooperate each other to maintain liver homeostasis. However, the complexity and molecular mechanisms underlying the crosstalk between these different cell types remain to be revealed. Here, we generated mice with conditional deletion of Bmp9/10 in different liver cell types and demonstrated that HSCs was the major source of BMP9 and BMP10 in the liver. Using transgenic ALK1 (receptor for BMP9/10) reporter mice, we found that ALK1 is expressed on KCs and ECs other than HCs and HSCs. KCs from Bmp9/10HSC-KO (conditional deletion of Bmp9/10 from HSCs) mice lost their signature genes expression, such as ID1/3, CLEC4F, VSIG4 and CLEC2, and were replaced by monocyte-derived macrophages. ECs from Bmp9/10HSC-KO mice also lost their identity and were transdifferentiated to continuous ECs, ultimately leading to collagen IV deposition and liver fibrosis. Hepatic ECs expressed several angiocrine factors, such as BMP2, BMP6, Wnt2 and Rspo3, to regulate liver iron metabolism and metabolic zonation. We found that these angiocrine factors were significantly decreased in ECs from Bmp9/10HSC-KO mice, which further resulted in liver iron overload and disruption of HCs zonation. In addition, focal fatty liver spontaneously occurred in Bmp9/10HSC-KO mice at the age of 28W. In summary, we demonstrated that HSCs play a central role in mediating liver cell-cell crosstalk via production of BMP9/10 to maintain liver health.

2024-09-26 | GSE244429 | GEO

Stimulation of HUVEC by BMP9/10

Project description:The experiment monitors the response of human umbilical vein endothelial cells to stimulation with BMP9 and BMP10

2021-02-05 | GSE160023 | GEO