Endothelial to haematopoietic transition contributes to pulmonary arterial hypertension.

ABSTRACT:

Aims

The pathogenic mechanisms of pulmonary arterial hypertension (PAH) remain unclear, but involve dysfunctional endothelial cells (ECs), dysregulated immunity and inflammation in the lung. We hypothesize that a developmental process called endothelial to haematopoietic transition (EHT) contributes to the pathogenesis of pulmonary hypertension (PH). We sought to determine the role of EHT in mouse models of PH, to characterize specific cell types involved in this process, and to identify potential therapeutic targets to prevent disease progression.

Methods and results

When transgenic mice with fluorescence protein ZsGreen-labelled ECs were treated with Sugen/hypoxia (Su/Hx) combination to induce PH, the percentage of ZsGreen+ haematopoietic cells in the peripheral blood, pri

SUBMITTER: Liang OD 

PROVIDER: S-EPMC5852529 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature