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.
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.
Project description:To identify potential biological targets of the TGFβ pathway involved in AVM formation, we performed ChIP-sequencing experiments on BMP9 stimulated Ms1 endothelial cells (ECs). This data provides a comprehensive list of all SMAD4 binding sites in endothelial cells.
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.
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).
Project description:HUVEC were left untreated or stimulated for 5h with 2 ng/ml TNF. Comparsion of the gene profiles revealed TNF-mediated gene expression changes in HUVEC. Keywords: parallel sample
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.
