Transcriptional analysis of the impact of BMPR2 loss and BMP9 treatment on pulmonary artery endothelial cells
Pulmonary arterial hypertension (PAH) is a disease of the pulmonary endothelium associated with mutations in BMPR2, the gene encoding the bone morphogenetic protein (BMP) type II receptor (BMPR-II). Loss of BMPR-II in the pulmonary endothelium has been shown to alter the functional response of the endothelium to BMP9 treatment from growth suppression in healthy cells, to hyperproliferation with the loss of BMPR-II. To investigate the molecular mechanisms underlying this phenotypic switch, we performed RNA sequencing on total RNA isolated from primary human pulmonary artery endothelial cells treated with or without BMP9 following BMPR2 knockdown or control. Overall design: To investigate the role of BMPR2 loss and BMP9 treatment in the pulmonary endothelium, primary human pulmonary artery endothelial cells (HPAECs) were treated with or without 1ng/mL of BMP9 for 24 hours following the siRNA mediated knockdown of BMPR2 or control siRNA treatment.