Macrophage A2aR Alleviates LPS-Induced Vascular Endothelial Injury and Inflammation via Inhibiting M1 Polarisation and Oxidative Stress.

ABSTRACT: Vascular inflammation and endothelial dysfunction secondary to unchecked activation of endothelium are key mechanisms underlying sepsis and organ failure. However, the intrinsic processes that mitigate excessive endothelial cell activation remain incompletely understood. To determine the central role of adenosine A2a receptor (A2aR) on macrophages in modulating lipopolysaccharide (LPS)-induced vascular endothelial dysfunction, we constructed macrophage A2aR-conditional knockout (Mac-A2aR KO) mice, and stimulated the mice and macrophages with LPS. A2aR agonist, CGS21680, was administered to these models to further explore its impact. Results showed that knockout of Macrophage A2aR exacerbated LPS-induced vascular permeability, oedema, inflammatory cardiac damage and upregulated expression o

SUBMITTER: Li Y 

PROVIDER: S-EPMC11882390 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature