Dataset Information


Effects of BMPR2 Loss in Human Pulmonary Artery Endothelial Cells

ABSTRACT: 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.

ORGANISM(S): Homo sapiens  

SUBMITTER: Keytam Awad   Robert Danner  Jason Elinoff  Gabriela Ferreyra  Gabriela A Ferreyra 

PROVIDER: E-GEOD-70456 | ArrayExpress | 2015-12-04



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Raf/ERK drives the proliferative and invasive phenotype of BMPR2-silenced pulmonary artery endothelial cells.

Awad Keytam S KS   Elinoff Jason M JM   Wang Shuibang S   Gairhe Salina S   Ferreyra Gabriela A GA   Cai Rongman R   Sun Junfeng J   Solomon Michael A MA   Danner Robert L RL  

American journal of physiology. Lung cellular and molecular physiology 20151120 2

A proliferative endothelial cell phenotype, inflammation, and pulmonary vascular remodeling are prominent features of pulmonary arterial hypertension (PAH). Bone morphogenetic protein type II receptor (BMPR2) loss-of-function is the most common cause of heritable PAH and has been closely linked to the formation of pathological plexiform lesions. Although some BMPR2 mutations leave ligand-dependent responses intact, the disruption of ligand-independent, noncanonical functions are universal among  ...[more]

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