Renin-angiotensin system regulates pulmonary arterial smooth muscle cell migration in chronic thromboembolic pulmonary hypertension

Pulmonary arterial smooth muscle cell (PASMC) migration plays a key role in vascular remodeling which occurs during development of chronic thromboembolic pulmonary hypertension (CTEPH). Activation of the renin-angiotensin system (RAS) contributes to vascular remodeling observed in many diseases including idiopathic pulmonary arterial hypertension. However, the role of RAS imbalance in CTEPH has not been characterized. Here, we hypothesize that RAS imbalance regulates vascular remodeling by promoting PASMC migration in CTEPH. Serum renin and angiotensin II levels in CTEPH patients were quantified by ELISA. The pulmonary endarterectomy tissues were stained and analyzed by immunohistochemistry. PASMC were isolated and verified by immunofluorescence staining. PASMC migration was determined by the Transwell assay. Phosphorylation and protein level were detected by Western blotting.Serum levels of renin and angiotensin II were increased in CTEPH patients [renin (pg/ml) 1199.94 (690.85, 1656.90) vs. 595.43 (351.48，936.43), P