Project description:To identify CLIC4 effectors by studying proteins expressiosn altered by CLIC4 overexpression in human pulmonary artery endothelial cells.
Project description:Expression analysis of genes potentially regulated by BMPRII and beta-catenin. BMPRII has been linked as a genetic factor to the disease pulmonary arterial hypertension. Comparison of total mRNA obtained from human pulmonary artery endothelial cells treated with control, bone morphogentic protein receptor II, or beta-catenin siRNA
Project description:This data set provides different RNA expression data for primary human pulmonary endothelial cells with and without FXN deficiency achieved by RNAi transfection in an effort to understand the endothelial-specific effects of acquired frataxin (FXN) deficiency and their implications for pulmonary vascular disease.
Project description:Evaluation of microRNAs that are downstream of apelin/APJ signaling in the pulmonary artery endothelial cells. Triplicates per group, subjected to: 1) control siRNA, 2) apelin siRNA, 3) APJ siRNA, 4) apelin + APJ siRNA
Project description:Pulmonary arterial hypertension (PAH) is a fatal disease characterized by a proliferative endothelial cell phenotype, inflammation and pulmonary vascular remodeling. BMPR2 loss-of-function has been linked to pathologic plexiform lesions with obliteration of distal pulmonary arteries distal pulmonary arteries BMPR2 silencing inprimary human pulmonary artery ECs (HPAECs) recapitulate important aspects of cellular dysfunction and deregulated signaling associated with PAH. Primary HPAECs were transfected with gene-specific siRNA pools targeting BMPR2 or control siRNA followed PMA or control stimulation.
Project description:RAD21 ChIA-PET in human pulmonary artery endothelial cell For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
Project description:Pulmonary arterial hypertension (PAH) is a fatal disease characterized by a proliferative endothelial cell phenotype, inflammation and pulmonary vascular remodeling. BMPR2 loss-of-function has been linked to pathologic plexiform lesions with obliteration of distal pulmonary arteries distal pulmonary arteries BMPR2 silencing inprimary human pulmonary artery ECs (HPAECs) recapitulate important aspects of cellular dysfunction and deregulated signaling associated with PAH.
Project description:Pulmonary artery smooth muscle cells were either mock transfected, transfected with scramble control or transfected with pre-miR-143. Then miR-143 enriched exosmes were extracted from the PASMCs and put onto pulmonary arterial endothelial cells. After 24 hours the cells were harvested with Qiazol and processed for a microarray experiment. The experiment was performed in order to identify potential targets of miR-143.