Center for Biomolecular and Tissue Engineering Center for Biomolecular and Tissue Engineering
Pratt School of Engineering
Duke University

 HOME > pratt > CBTE    Search Help Login 

Publications [#162870] of Christopher D. Kontos

Papers Published

  1. A Ahmed, T Fujisawa, XL Niu, S Ahmad, B Al-Ani, K Chudasama, A Abbas, R Potluri, V Bhandari, CM Findley, GK Lam, J Huang, PW Hewett, M Cudmore, CD Kontos, Angiopoietin-2 confers Atheroprotection in apoE-/- mice by inhibiting LDL oxidation via nitric oxide., Circulation research, vol. 104 no. 12 (June, 2009), pp. 1333-6, ISSN 1524-4571 [doi]
    (last updated on 2013/05/16)

    Abstract:
    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.

    Keywords:
    Adenoviridae • Angiopoietin-2 • Animals • Apolipoproteins E* • Atherosclerosis • Endothelial Cells • Endothelium, Vascular • Female • Lipoproteins, LDL • Male • Mice • Mice, Knockout • Neovascularization, Physiologic • Nitric Oxide • Nitric Oxide Synthase Type III • Oxidation-Reduction • Receptor, TIE-2 • Transduction, Genetic • Vasculitis • biosynthesis • genetics • metabolism • metabolism* • prevention & control


Duke University * Pratt * CBTE * Reload * Login
x