Angiopoietin-2 confers Atheroprotection in apoE-/- mice by inhibiting LDL oxidation via nitric oxide
| Autor: | Christopher D. Kontos, Asif Ahmed, Jianhua Huang, Xi-Lin Niu, Peter W. Hewett, Rahul Potluri, Takeshi Fujisawa, Kunal Chudasama, Melissa J. Cudmore, Bahjat Al-Ani, Clarence M. Findley, Allyah Abbas, Shakil Ahmad, Vineet Bhandari, Gregory K.W. Lam |
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| Rok vydání: | 2009 |
| Předmět: |
Male
Vasculitis medicine.medical_specialty Endothelium Nitric Oxide Synthase Type III Physiology Angiogenesis Neovascularization Physiologic Biology Endothelial NOS Nitric Oxide Article Nitric oxide Adenoviridae Angiopoietin Angiopoietin-2 chemistry.chemical_compound Mice Apolipoproteins E Transduction Genetic Internal medicine medicine Animals Mice Knockout Endothelial Cells Atherosclerosis Receptor TIE-2 Nitric oxide synthase Endothelial stem cell Lipoproteins LDL Endocrinology medicine.anatomical_structure chemistry biology.protein cardiovascular system Female Endothelium Vascular Cardiology and Cardiovascular Medicine Oxidation-Reduction |
| Zdroj: | Ahmed, A, Fujisawa, T, Niu, X-L, Ahmad, S, Al-Ani, B, Chudasama, K, Abbas, A, Potluri, R, Bhandari, V, Findley, C M, Lam, G K W, Huang, J, Hewett, P W, Cudmore, M & Kontos, C D 2009, ' Angiopoietin-2 confers Atheroprotection in apoE-/-mice by inhibiting LDL oxidation via nitric oxide ', Circulation Research, vol. 104, no. 12, pp. 1333-6 . https://doi.org/10.1161/CIRCRESAHA.109.196154 |
| ISSN: | 1524-4571 |
| DOI: | 10.1161/CIRCRESAHA.109.196154 |
| Popis: | 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 (≈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. |
| Databáze: | OpenAIRE |
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