Basal ATP release signals through the P2Y₂ receptor to maintain the differentiated phenotype of vascular smooth muscle cells.

ABSTRACT:

Background and aims

Vascular smooth muscle cell (VSMC) dedifferentiation contributes substantively to vascular disease. VSMCs spontaneously release low levels of ATP that modulate vessel contractility, but it is unclear if autocrine ATP signaling in VSMCs is critical to the maintenance of the VSMC contractile phenotype.

Methods

We used pharmacological inhibitors to block ATP release in human aortic smooth muscle cells (HASMCs) for studying changes in VSMC differentiation marker gene expression. We employed RNA interference and generated mice with SMC-specific inducible deletion of the P2Y₂ receptor (P2Y₂R) gene to evaluate resulting phenotypic alterations.

Results

HASMCs constitutively release low levels of ATP that when blocked results in a sign

SUBMITTER: Chen X 

PROVIDER: S-EPMC11254552 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature