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Gene expression analysis of pulmonary artery in a rabbit model of pulmonary thromboembolism

ABSTRACT: Acute pulmonary thromboembolism (PTE) refers to the obstruction of the pulmonary artery or its branches by thrombus. Recent studies suggest that PTE-induced endothelium injury is the major physiological consequence of PTE, and PTE-induced endothelium injury can be used to stratify disease severity. Several plasma biomarkers have been identified in PTE patients, but genome-wide gene expression has not been attempted in PTE. In this study, using rabbit autologous thrombus PTE model, we applied gene expression array to identify genes and proteins changes in pulmonary arteries under PTE.

ORGANISM(S): Oryctolagus cuniculus

PROVIDER: GSE84738 | GEO | 2016/07/23

SECONDARY ACCESSION(S): PRJNA330975

REPOSITORIES: GEO

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Project description:Dysfunction of pulmonary arterial endothelial cells (PAECs) is associated with the development and progression of vascular pathology. However, it remains unknown how pulmonary hypertension (PH) affects cellular composition and transcriptomic profile of pulmonary endothelium. Here, we have undertaken a single-cell, compartment specific approach to characterise alterations in PAECs associated with two different types of PH, i.e., pulmonary arterial hypertension (PAH) and pulmonary hypertension associated with pulmonary fibrosis (PHPF). Our unbiased analysis showed that endothelium of medium / small caliber pulmonary arteries is composed of three subsets of endothelial cells (ECs). The analysis of healthy and PH endothelium revealed that the three populations are persistently represented in remodelled arteries. Additionally, an exploratory analysis of human aorta (AO) and coronary arteries (CA) endothelium revealed that, although similar gene expression patterns were noticeable, PAECs subpopulations proportions differs significantly from pulmonary arteries (PA) endothelium. To address whether EC heterogeneity is a prime feature of human endothelium, we also performed a similar analysis in a murine model of hypoxia, revealing that similar EC populations were evident in this animal model. Comparative analysis of EC subpopulations in healthy and PH EC identified a common genetic deregulation accompanying vascular remodelling. Even though murine EC displayed some similarities with human EC subpopulations, the intense re-programming associated with hypoxia associated vascular remodelling displayed significant differences compared to the human disease. Finally, in depth comparative analysis of PAH and PHPF EC highlighted the development of disease-specific transcriptomic alterations in the three populations. Therefore, characterisation of transcriptomic differences in the endothelial bed of PAH and PHPF patients can facilitate identification of novel, disease-specific therapeutic targets.

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Gene expression analysis of pulmonary artery in a rabbit model of pulmonary thromboembolism

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