Literature DB >> 21411092

Role for Nox1 NADPH oxidase in atherosclerosis.

Andrea L Sheehan1, Samuel Carrell, Bryon Johnson, Bojana Stanic, Botond Banfi, Francis J Miller.   

Abstract

OBJECTIVE: Examine the contribution of Nox1 NADPH oxidase to atherogenesis. METHODS AND
RESULTS: Male apolipoprotein E deficient mice (ApoE(-/-)) and male mice deficient in both apolipoprotein E and Nox1 (ApoE(-/-) Nox1(-/y)) received an atherogenic diet for 18 weeks. Mean blood pressures, body weights, and serum cholesterol levels were similar between the two groups of mice. Deficiency of Nox1 decreased superoxide levels and reduced lesion area in the aortic arch from 43% (ApoE(-/-)) to 28% (ApoE(-/-) Nox1(-/y)). The reduction in lesion size at the level of the aortic valve in ApoE(-/-)/Nox1(-/y) was accompanied by a decrease in macrophage infiltration as compared to ApoE(-/-) mice. Carotid artery ligation in ApoE(-/-) mice induced accelerated intimal hyperplasia with decreased cellular proliferation and increased collagen content in the neointima of vessels deficient in Nox1.
CONCLUSIONS: Nox1-derived ROS modify lesion composition and contribute to lesion size in a murine model of atherosclerosis. Published by Elsevier Ireland Ltd.

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Year:  2011        PMID: 21411092      PMCID: PMC3110523          DOI: 10.1016/j.atherosclerosis.2011.02.028

Source DB:  PubMed          Journal:  Atherosclerosis        ISSN: 0021-9150            Impact factor:   5.162


  38 in total

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