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The article reports on the study which focuses on the function of Angiopoietin (Ang)-2 in the maintenance of large vessels. It states that Ang-2, which is a key regulator of angiogenesis, suppresses atherosclerosis in apoE-Null mice by inhibiting low density lipoproteins (LDL) oxidation via nitric oxide (NO). It further notes that vascular inflammation and hypercholesterolemia promotes atherosclerosis.

Atherosclerosis is promoted by a combination of hypercholesterolemia and vascular inflammation. The function of Angiopoietin (Ang)-2, a key regulator of angiogenesis, in the maintenance of large vessels is unknown. A single systemic administration of Ang-2 adenovirus (AdAng-2) to apoE(-/-) mice fed a Western diet significantly reduced atherosclerotic lesion size ( approximately 40%) and oxidized LDL and macrophage content of the plaques. These beneficial effects were abolished by the inhibition of nitric oxide synthase (NOS). In endothelial cells, endothelial NOS activation per se inhibited LDL oxidation and Ang-2 stimulated NO release in a Tie2-dependent manner to decrease LDL oxidation. These findings demonstrate a novel atheroprotective role for Ang-2 when endothelial cell function is compromised and suggest that growth factors, which stimulate NO release without inducing inflammation, could offer atheroprotection.