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Investigation of endothelial cell gene dysregulation in early pulmonary arterial hypertension disease model

ABSTRACT: Endothelial cell (EC) dysfunction plays a key role in the pathogenesis of pulmonary arterial hypertension (PAH). To avoid cell cultures and whole lung tissue samples, we have, for the first time, used CD31 antibody coated magnetic beads in conjunction with genome scale RNA expression microarrays to profile ECs in vivo at any stage of PAH. We hypothesized that targeting early stages of the disease would identify novel mediators of PAH and genes linked to bone morphogenetic protein receptor 2 (BMPR2) signaling. Rats were treated with either monocrotaline (60mg/kg) or saline as control with 4 animals in each experimental group. Gene expression profiling was performed on primary pulmonary endothelial cells directly after isolation from whole lung tissue 5 days after treatment.

ORGANISM(S): Rattus norvegicus  

SUBMITTER: Tero-Pekka Alastalo   Sanna Vattulainen  Molong Li 

PROVIDER: E-GEOD-42767 | ArrayExpress | 2014-02-06



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Loss of bone morphogenetic protein receptor 2 is associated with abnormal DNA repair in pulmonary arterial hypertension.

Li Molong M   Vattulainen Sanna S   Aho Joonas J   Orcholski Marc M   Rojas Vanessa V   Yuan Ke K   Helenius Mikko M   Taimen Pekka P   Myllykangas Samuel S   De Jesus Perez Vinicio V   Koskenvuo Juha W JW   Alastalo Tero-Pekka TP  

American journal of respiratory cell and molecular biology 20140601 6

Occlusive vasculopathy with intimal hyperplasia and plexogenic arteriopathy are severe histopathological changes characteristic of pulmonary arterial hypertension (PAH). Although a phenotypic switch in pulmonary endothelial cells (ECs) has been suggested to play a critical role in the formation of occlusive lesions, the pathobiology of this process is poorly understood. The goal of this study was to identify novel molecular mechanisms associated with EC dysfunction and PAH-associated bone morpho  ...[more]

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