Atheroprone flow activates inflammation via endothelial ATP-dependent P2X7-p38 signalling.

ABSTRACT:

Objective

Atherosclerosis is a focal disease occurring at arterial sites of disturbed blood flow that generates low oscillating shear stress. Endothelial inflammatory signalling is enhanced at sites of disturbed flow via mechanisms that are incompletely understood. The influence of disturbed flow on endothelial adenosine triphosphate (ATP) receptors and downstream signalling was assessed.

Methods and results

Cultured human endothelial cells were exposed to atheroprotective (high uniform) or atheroprone (low oscillatory) shear stress for 72 h prior to assessment of ATP responses. Imaging of cells loaded with a calcium-sensitive fluorescent dye revealed that atheroprone flow enhanced extracellular calcium influx in response to 300 µM 2'(3')-O-(4-Benzoylbenzoyl) adenosine-5'-tr

SUBMITTER: Green JP 

PROVIDER: S-EPMC5852506 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature