Induced Endothelial Cell Cycle Arrest Prevents Arterio-venous Malformations in Hereditary Hemorrhagic Telangiectasia (Bulk RNA-Seq)

Distinct endothelial cell cycle states (early G1 vs. late G1) provide different “windows of opportunity” to enable the differential expression of genes that regulate venous and arterial specification, respectively. Endothelial cell cycle control and arterial-venous identities are disrupted in vascular malformations including arteriovenous (AV) shunts which is a hallmark of hereditary hemorrhagic telangiectasia (HHT). We show how endothelial cell late G1 arrest induced by Palbociclib modulates the expression of genes regulating arterio-venous identity and prevents AVM development induced by BMP9/10 inhibition. Overall design: Eyes from P7 pups of control (group 1), BMP9/10 Abs-treated (group 2), and BMP9/10 Abs + CDK4/6i (group 3) treated animals were dissected out and primary retinal ECs were FACS-isolated and prepared for bulk RNA sequencing of total RNA.