Project description:To identify CLIC4 effectors by studying proteins expressiosn altered by CLIC4 overexpression in human pulmonary artery endothelial cells.
Project description:Sprague Dawley rats were treated with monocrotaline 60 mg/kg by intraperitoneal injection or vehicle control on day 0. On day 23, animals were sacrificed and pulmonary artery endothelial cells (PAECs) were isolated for transcriptomic analysis.
Project description:Transcriptional profiling of human pulmonary artery endothelial (HAPEC) and smooth muscle (PASM) cells comparing control untreated cells with cells transfected with ARSB-siRNA. Goal was to determine the effects of silenced of arylsufatase B on global gene expression in HAPEC and PASM cells.
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:Pulmonary Hypertension (PH) is a frequent complication of Pulmonary Fibrosis (PF). PH can be seen in PF in the abscence of hypoxemia, irrespective of the degree of fibrosis. At the same time, a consistent number of patients with advanced PF never develop PH. The pathogenesis of PH secondary to PF remains unclear. PF patients are often referred to lung transplantation, but they present a higher incidence of pimary graft dysfunction than other diseases. The cause of this is unknown, and the relationship with PH remains unclear. We used microarray to identifiy the gene expression profiles in PF patients with and without PH Fresh frozen lung samples were obtained from the recipients organs of 116 PF patients undergoing lung transplantation. RNA was extracted and hybridized on Affymetrix microarrays. Pulmonary artery pressures were recorded intraoperatively with right heart catheters before starting lung transplantation. Patients were divided in different groups based on the mean pulmonary artery pressure. We compared the gene expression profiles in the group with severe PH (mPAP>40 mmHg, n=17) and in that without PH (mPAP<20 mmHg, n=22)) and obtained a gene signature, which was used for clusterying analysis. The clustering analysis based on the gene signature was then validated in an Intermediate PH group (mPAP 21-39 mmHg, n=45) and in a Validation Set (n=32).
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.