Endogenous hydrogen sulfide persulfidates endothelin type A receptor to inhibit pulmonary arterial smooth muscle cell proliferation.

ABSTRACT:

Background

The binding of endothelin-1 (ET-1) to endothelin type A receptor (ETAR) performs a critical action in pulmonary arterial smooth muscle cell (PASMC) proliferation leading to pulmonary vascular structural remodeling. More evidence showed that cystathionine γ-lyase (CSE)-catalyzed endogenous hydrogen sulfide (H₂S) was involved in the pathogenesis of cardiovascular diseases. In this study, we aimed to explore the effect of endogenous H₂S/CSE pathway on the ET-1/ETAR binding and its underlying mechanisms in the cellular and animal models of PASMC proliferation.

Methods and results

Both live cell imaging and ligand-receptor assays revealed that H₂S donor, NaHS, inhibited the binding of ET-1/ETAR in human PASMCs (HPASMCs) and HEK-293A cel

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC11787542 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature