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: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:Bone morphogenetic protein (BMP) signaling and fluid shear stress (FSS), the frictional force exerted on endothelial cells by blood flowing over them, have complementary functions in vascular homeostasis and disease development. Both induce a wide range of target genes, not only independently but also in a synergistic or antagonistic manner. Despite thorough research into genetic regulation downstream of BMP9 and FSS, detailed information on how both regulate chromatin accessibility is still missing. Here, we investigated whether BMP9 and FSS act independently, synergistically, or antagonistically in chromatin remodeling. To this end, we employed Assay for Transposase-Accessible Chromatin followed by sequencing (ATAC-seq) to analyze arterial endothelial cells stimulated with BMP9 and FSS either individually or in combination.
Project description:To identify potential target genes regulated by BMP9 in MSCs, we used microarray to profile expression patterns of BMP9- vs. GFP-stimulated MSCs.
Project description:BMP9 signaling has been implicated in hereditary hemorrhagic telangiectasia and vascular remodeling, acting via the HHT target genes, endoglin and ALK1. This study sought to identify endothelial BMP9-regulated proteins that could affect the HHT phenotype. Gene ontology analysis of cDNA microarray data obtained following BMP9 treatment of primary human endothelial cells indicated regulation of chemokine, adhesion, and inflammation pathways. The sample set is comprised of three biological replicate control human dermal microvascular endothelial cells, and three treated (5 ng/ml human recombinant BMP9) biological replicate human dermal microvascular endothelial cells
Project description:To identify potential target genes regulated by BMP9 in MSCs, we used microarray to profile expression patterns of BMP9- vs. GFP-stimulated MSCs. Subconfluent mouse C3H10T1/2 cells were transduced with adenoviral vector expressing BMP9 or GFP for 30h. Total RNA was isolated for microarray analysis using Affymetrix mouse MOE430A GeneChips. Experiments were done in triplicate.
Project description:BMP9 signaling has been implicated in hereditary hemorrhagic telangiectasia and vascular remodeling, acting via the HHT target genes, endoglin and ALK1. This study sought to identify endothelial BMP9-regulated proteins that could affect the HHT phenotype. Gene ontology analysis of cDNA microarray data obtained following BMP9 treatment of primary human endothelial cells indicated regulation of chemokine, adhesion, and inflammation pathways.
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.