Differential effects of diabetes on the expression of the gp91phox homologues nox1 and nox4 - PubMed (original) (raw)
. 2005 Aug 1;39(3):381-91.
doi: 10.1016/j.freeradbiomed.2005.03.020. Epub 2005 Apr 7.
Andreas Daiber, Andrei L Kleschyov, Alexander Mülsch, Karsten Sydow, Eberhard Schulz, Kai Chen, John F Keaney Jr, Bernard Lassègue, Ulrich Walter, Kathy K Griendling, Thomas Münzel
Affiliations
- PMID: 15993337
- DOI: 10.1016/j.freeradbiomed.2005.03.020
Differential effects of diabetes on the expression of the gp91phox homologues nox1 and nox4
Maria C Wendt et al. Free Radic Biol Med. 2005.
Abstract
The nox2-dependent NADPH oxidase was shown to be a major superoxide source in vascular disease, including diabetes. Smooth muscle cells of large arteries lack the phagocytic gp91phox subunit of the enzyme; however, two homologues have been identified in these cells, nox1 and nox4. It remained to be established whether also increases in protein levels of the nonphagocytic NADPH oxidase contribute to increased superoxide formation in diabetic vessels. To investigate changes in the expression of these homologues, we measured their expression in aortic vessels of type I diabetic rats. Eight weeks after streptozotocin treatment, we found a doubling in nox1 protein expression, while the expression of nox4 remained unchanged. This was associated with a significant increase in the NADPH oxidase activity in membrane fractions of diabetic heart and aortic tissue. Furthermore, we observed a decreased sensitivity of diabetic vessels to acetylcholine and nitroglycerin and a decrease in both acetylcholine-stimulated NO production and phosphorylation of VASP, despite an increase in endothelial NO synthase (NOSIII) expression. In addition, xanthine oxidase activity was markedly increased in plasma and 100,000 g supernatant of cardiac tissue of diabetic rats, while myocardial mitochondrial superoxide formation was only weakly enhanced. We conclude that in addition to phagocytic NADPH oxidase, also nonphagocytic, vascular NADPH oxidase subunit nox1, uncoupled NOSIII, and plasma xanthine oxidase contribute to endothelial dysfunction in the setting of diabetes mellitus.
Similar articles
- NADPH oxidase accounts for enhanced superoxide production and impaired endothelium-dependent smooth muscle relaxation in BKbeta1-/- mice.
Oelze M, Warnholtz A, Faulhaber J, Wenzel P, Kleschyov AL, Coldewey M, Hink U, Pongs O, Fleming I, Wassmann S, Meinertz T, Ehmke H, Daiber A, Münzel T. Oelze M, et al. Arterioscler Thromb Vasc Biol. 2006 Aug;26(8):1753-9. doi: 10.1161/01.ATV.0000231511.26860.50. Epub 2006 Jun 8. Arterioscler Thromb Vasc Biol. 2006. PMID: 16763163 - Increased oxidative stress in the streptozotocin-induced diabetic apoE-deficient mouse: changes in expression of NADPH oxidase subunits and eNOS.
Ding H, Hashem M, Triggle C. Ding H, et al. Eur J Pharmacol. 2007 Apr 30;561(1-3):121-8. doi: 10.1016/j.ejphar.2006.12.034. Epub 2007 Jan 20. Eur J Pharmacol. 2007. PMID: 17292348 - The contribution of Nox4 to NADPH oxidase activity in mouse vascular smooth muscle.
Ellmark SH, Dusting GJ, Fui MN, Guzzo-Pernell N, Drummond GR. Ellmark SH, et al. Cardiovasc Res. 2005 Feb 1;65(2):495-504. doi: 10.1016/j.cardiores.2004.10.026. Cardiovasc Res. 2005. PMID: 15639489 - NADPH oxidases, reactive oxygen species, and hypertension: clinical implications and therapeutic possibilities.
Paravicini TM, Touyz RM. Paravicini TM, et al. Diabetes Care. 2008 Feb;31 Suppl 2:S170-80. doi: 10.2337/dc08-s247. Diabetes Care. 2008. PMID: 18227481 Review. - Novel isoforms of NADPH oxidase in vascular physiology and pathophysiology.
Bengtsson SH, Gulluyan LM, Dusting GJ, Drummond GR. Bengtsson SH, et al. Clin Exp Pharmacol Physiol. 2003 Nov;30(11):849-54. doi: 10.1046/j.1440-1681.2003.03929.x. Clin Exp Pharmacol Physiol. 2003. PMID: 14678249 Review.
Cited by
- Blockade of TGF-β 1 signalling inhibits cardiac NADPH oxidase overactivity in hypertensive rats.
Miguel-Carrasco JL, Baltanás A, Cebrián C, Moreno MU, López B, Hermida N, González A, Dotor J, Borrás-Cuesta F, Díez J, Fortuño A, Zalba G. Miguel-Carrasco JL, et al. Oxid Med Cell Longev. 2012;2012:726940. doi: 10.1155/2012/726940. Epub 2012 Jun 3. Oxid Med Cell Longev. 2012. PMID: 22701756 Free PMC article. - Regulation of Vascular Function and Inflammation via Cross Talk of Reactive Oxygen and Nitrogen Species from Mitochondria or NADPH Oxidase-Implications for Diabetes Progression.
Daiber A, Steven S, Vujacic-Mirski K, Kalinovic S, Oelze M, Di Lisa F, Münzel T. Daiber A, et al. Int J Mol Sci. 2020 May 12;21(10):3405. doi: 10.3390/ijms21103405. Int J Mol Sci. 2020. PMID: 32408480 Free PMC article. Review. - Pentaerythritol Tetranitrate In Vivo Treatment Improves Oxidative Stress and Vascular Dysfunction by Suppression of Endothelin-1 Signaling in Monocrotaline-Induced Pulmonary Hypertension.
Steven S, Oelze M, Brandt M, Ullmann E, Kröller-Schön S, Heeren T, Tran LP, Daub S, Dib M, Stalleicken D, Wenzel P, Münzel T, Daiber A. Steven S, et al. Oxid Med Cell Longev. 2017;2017:4353462. doi: 10.1155/2017/4353462. Epub 2017 Feb 28. Oxid Med Cell Longev. 2017. PMID: 28337251 Free PMC article. - NADPH oxidases are responsible for the failure of nitric oxide to inhibit migration of smooth muscle cells exposed to high glucose.
Tong X, Schröder K. Tong X, et al. Free Radic Biol Med. 2009 Dec 1;47(11):1578-83. doi: 10.1016/j.freeradbiomed.2009.08.026. Epub 2009 Sep 3. Free Radic Biol Med. 2009. PMID: 19733235 Free PMC article. - NADPH oxidases: functions and pathologies in the vasculature.
Lassègue B, Griendling KK. Lassègue B, et al. Arterioscler Thromb Vasc Biol. 2010 Apr;30(4):653-61. doi: 10.1161/ATVBAHA.108.181610. Epub 2009 Nov 12. Arterioscler Thromb Vasc Biol. 2010. PMID: 19910640 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Miscellaneous