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Genome-wide analysis of human pulmonary artery endothelial cells after knockdown of either BMPRII or beta-catenin

ABSTRACT: Expression analysis of genes potentially regulated by BMPRII and beta-catenin. BMPRII has been linked as a genetic factor to the disease pulmonary arterial hypertension.

ORGANISM(S): Homo sapiens

PROVIDER: GSE18956 | GEO | 2010/11/06

SECONDARY ACCESSION(S): PRJNA120991

REPOSITORIES: GEO

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Genome-wide analysis of human pulmonary artery endothelial cells after knockdown of either BMPRII or beta-catenin

Project description:Expression analysis of genes potentially regulated by BMPRII and beta-catenin. BMPRII has been linked as a genetic factor to the disease pulmonary arterial hypertension. Comparison of total mRNA obtained from human pulmonary artery endothelial cells treated with control, bone morphogentic protein receptor II, or beta-catenin siRNA

2010-11-06 | E-GEOD-18956 | biostudies-arrayexpress

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ChIP-chip of BMP2 or control treated human pulmonary artery endothelial cells with anti-beta-catenin or anti-ppar-gamma antibodies on promoter regions

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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.

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ChIP-chip of BMP2 or control treated human pulmonary artery endothelial cells with anti-beta-catenin or anti-ppar-gamma antibodies on promoter regions

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Analysis of Differentially Regulated Genes in Lung Tissue

Project description:Pulmonary arterial hypertension (PAH) is a progressive fatal disease that is characterized by pathological pulmonary artery remodeling, in which endothelial cell (EC) dysfunction is critically involved. We herein describe a previously unknown role of endothelial angiocrine in pulmonary hypertension. By searching for genes highly expressed in lung microvascular ECs, we identified inhibin--A (INHBA) as an angiocrine factor produced by pulmonary capillaries. We found that excess production of INHBA by ECs impairs the endothelial function in an autocrine manner by functioning as activin A (ActA). Mechanistically, ActA induces bone morphogenetic protein receptor type 2 (BMPRII) internalization and targeting to lysosomes for degradation, resulting in BMPRII signal deficiency in ECs. When endothelial ActA-BMPRII link is overdriven in mice, hypoxia-induced pulmonary hypertension was exacerbated, whereas conditional knockout of INHBA in ECs prevents the progression of pulmonary hypertension. These data collectively indicate a critical role for the dysregulated endothelial ActA-BMPRII link in the progression of pulmonary hypertension, and thus endothelial INHBA/ActA is an attractive pharmacotherapeutic target for the treatment of PAH.

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Transcriptomics and proteomics revealed sex differences in human pulmonary microvascular endothelial cells

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