NDLI: Augmented superoxide production by Nox2-containing NADPH oxidase causes cerebral artery dysfunction during hypercholesterolemia.

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Augmented superoxide production by Nox2-containing NADPH oxidase causes cerebral artery dysfunction during hypercholesterolemia.

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Augmented superoxide production by Nox2-containing NADPH oxidase causes cerebral artery dysfunction during hypercholesterolemia.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Miller, Alyson A. Diep, Henry De Silva, T. Michael Sobey, Christopher G. Judkins, Courtney P. Drummond, Grant R.
Description	Country affiliation: Australia Author Affiliation: Miller AA ( Department of Pharmacology, Monash University, Clayton, Victoria, Australia. alyson.miller@med.monash.edu.au)
Abstract	BACKGROUND AND PURPOSE: We tested the hypothesis that elevated superoxide production by Nox2-NADPH oxidase occurs in cerebral arteries during hypercholesterolemia and causes decreased nitric oxide function. METHODS: Wild-type (WT), apolipoprotein E-deficient (ApoE(-/-)) and Nox2(-/-)/ApoE(-/-) mice were fed a high-fat diet for 7 to 14 weeks. Basal superoxide production by cerebral arteries was measured using L-012 (100 micromol/L)-enhanced chemiluminescence. Nitric oxide function was assessed in isolated middle cerebral arteries through the constrictor response to N(omega)-nitro-L-arginine methyl ester (L-NAME; 100 micromol/L). Western blotting was used to measure protein expression of Nox2, p47phox, endothelial nitric oxide synthase, and superoxide dismutases (1-3). RESULTS: Morphology of cerebral arteries was similar in WT and ApoE(-/-) mice. In ApoE(-/-), but not Nox2(-/-)/ApoE(-/-) mice, superoxide production by cerebral arteries was approximately 50% greater than in WT mice (P<0.05). Moreover, the magnitude of L-NAME-induced contractions of isolated middle cerebral arteries from ApoE(-/-) mice was <50% of that in WT mice (P<0.05), whereas in Nox2(-/-)/ApoE(-/-) mice, the contractile response was comparable to WT responses. In the presence of the superoxide scavenger, tempol (1 mmol/L), L-NAME-induced contractions of middle cerebral arteries were similar between WT and ApoE(-/-) mice. Expression of p47phox was approximately 2-fold higher in ApoE(-/-) versus WT mice, whereas Nox2, endothelial nitric oxide synthase, and superoxide dismutase isoforms were unchanged. CONCLUSIONS: Elevated superoxide production and reduced basal nitric oxide-mediated relaxation occur in cerebral arteries of hypercholesterolemic mice even in the absence of lesions. These changes appear to be exclusively due to increased activity of Nox2-NADPH oxidase, possibly through increased expression of its regulatory subunit p47phox.
ISSN	00392499
e-ISSN	15244628
Journal	Stroke
Issue Number	4
Volume Number	41
Language	English
Publisher	Lippincott Williams & Wilkins (on behalf of the American Heart Association)
Publisher Date	2010-04-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cerebral Arteries Metabolism Physiopathology Hypercholesterolemia Membrane Glycoproteins Nadph Oxidase Superoxides Animals Antioxidants Pharmacology Aorta Anatomy & Histology Pathology Apolipoproteins E Genetics Drug Effects Cholesterol Blood Cyclic N-oxides Dietary Fats Enzyme Inhibitors Antagonists & Inhibitors Mice Mice, Knockout Ng-nitroarginine Methyl Ester Nitric Oxide Spin Labels Vasoconstriction Physiology Research Support, Non-u.s. Gov't Discipline Cardiology
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine Neuroscience Advanced and Specialized Nursing Neurology (clinical)

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