Adenosine kinase is critical for neointima formation after vascular injury by inducing aberrant DNA hypermethylation.

ABSTRACT:

Aims

Adenosine receptors and extracellular adenosine have been demonstrated to modulate vascular smooth muscle cell (VSMC) proliferation and neointima formation. Adenosine kinase (ADK) is a major enzyme regulating intracellular adenosine levels but is function in VSMC remains unclear. Here, we investigated the role of ADK in vascular injury-induced smooth muscle proliferation and delineated the mechanisms underlying its action.

Methods and results

We found that ADK expression was higher in the neointima of injured vessels and in platelet-derived growth factor-treated VSMCs. Genetic and pharmacological inhibition of ADK was enough to attenuate arterial injury-induced neointima formation due to inhibition of VSMC proliferation. Mechanistically, using infinium methylation assay

SUBMITTER: Wang Y 

PROVIDER: S-EPMC7820850 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature