NADPH oxidase activity is higher in cerebral versus systemic arteries of four animal species: role of Nox2
- 1 January 2009
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Heart and Circulatory Physiology
- Vol. 296 (1), H220-H225
- https://doi.org/10.1152/ajpheart.00987.2008
Abstract
We previously reported that NADPH oxidase activity is greater in intracranial cerebral versus systemic arteries of the rat. Here, we first tested whether NADPH oxidase activity is also greater in intracranial cerebral than systemic arteries of three other animal species, i.e., mouse, rabbit, and pig. Second, using Nox2-deficient mice, we evaluated the involvement of Nox2-containing NADPH oxidases in any such regional differences. NADPH-stimulated superoxide (O2−) production by basilar, middle cerebral arteries (MCA), and common carotid arteries (CA) and thoracic aorta (AO) from rat, mouse, rabbit, and pig was measured using lucigenin-enhanced chemiluminescence. Basal production of O2− and hydrogen peroxide (H2O2) by cerebral arteries, AO, and CA from wild-type (WT) and Nox2−/− mice was measured using L-012-enhanced chemiluminescence and Amplex Red fluorescence, respectively. Western blotting was used to measure Nox2 and SOD1–3 protein expression, and immunofluorescence was used to localize Nox2, in mouse arteries. In rats, WT mice, rabbits, and pigs, NADPH-stimulated O2− production by cerebral arteries was up to 40-fold greater than that in AO and CA. In WT mice, basal O2− and H2O2 production by cerebral arteries was ninefold and ∼2.5-fold higher, respectively, than that in AO and CA and was associated with ∼40% greater expression of Nox2 protein. Nox2 immunofluorescence was localized to the endothelium, and to a lesser extent the adventitia, in all mouse arteries and appeared to be more intense in endothelium of MCA than AO or CA. In Nox2−/− mice, NADPH-stimulated O2− production by cerebral arteries was ∼35% lower than that in WT mice, whereas Nox2 deletion had no significant effect on O2− production by AO or CA. Thus NADPH oxidase activity is greater in intracranial cerebral versus systemic arteries of several animal species and is associated with higher cerebrovascular expression and activity of Nox2.Keywords
This publication has 27 references indexed in Scilit:
- NADPH Oxidase Plays a Central Role in Blood-Brain Barrier Damage in Experimental StrokeStroke, 2007
- EFFECT OF GENDER AND SEX HORMONES ON VASCULAR OXIDATIVE STRESSClinical and Experimental Pharmacology and Physiology, 2007
- Effect of Gender on NADPH-Oxidase Activity, Expression, and Function in the Cerebral CirculationStroke, 2007
- Parathyroid hormone treatment induces dissociation of type IIa Na+-Picotransporter-Na+/H+exchanger regulatory factor-1 complexesAmerican Journal of Physiology-Cell Physiology, 2005
- NAD(P)H Oxidases in Rat Basilar Arterial Endothelial CellsStroke, 2005
- Oxygen Glucose Deprivation Switches the Transport of tPA Across the Blood–Brain Barrier From an LRP-Dependent to an Increased LRP-Independent ProcessStroke, 2005
- Exogenous NADPH Increases Cerebral Blood Flow Through NADPH Oxidase–Dependent and –Independent MechanismsArteriosclerosis, Thrombosis, and Vascular Biology, 2004
- Increased NADPH-Oxidase Activity and Nox4 Expression During Chronic Hypertension Is Associated With Enhanced Cerebral Vasodilatation to NADPH In VivoStroke, 2004
- Induction of gp91-phox, a Component of the Phagocyte NADPH Oxidase, in Microglial Cells during Central Nervous System InflammationJournal of Cerebral Blood Flow & Metabolism, 2001
- A Novel Superoxide-producing NAD(P)H Oxidase in KidneyJournal of Biological Chemistry, 2001