The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Endothelial Nitric Oxide Synthase Uncoupling Impairs Endothelial Progenitor Cell Mobilization and Function in Diabetes
Abstract
Uncoupling of the endothelial nitric oxide synthase (eNOS) resulting in superoxide anion (O2−) formation instead of nitric oxide (NO) causes diabetic endothelial dysfunction. eNOS regulates mobilization and function of endothelial progenitor cells (EPCs), key regulators of vascular repair. We postulate a role of eNOS uncoupling for reduced number and function of EPC in diabetes. EPC levels in diabetic patients were significantly reduced compared with those of control subjects. EPCs from diabetic patients produced excessive O2− and showed impaired migratory capacity compared with nondiabetic control subjects. NOS inhibition with NG-nitro-l-arginine attenuated O2− production and normalized functional capacity of EPCs from diabetic patients. Glucose-mediated EPC dysfunction was protein kinase C dependent, associated with reduced intracellular BH4 (tetrahydrobiopterin) concentrations, and reversible after exogenous BH4 treatment. Activation of NADPH oxidases played an additional but minor role in glucose-mediated EPC dysfunction. In rats with streptozotocin-induced diabetes, circulating EPCs were reduced to 39 ± 5% of controls and associated with uncoupled eNOS in bone marrow. Our results identify uncoupling of eNOS in diabetic bone marrow, glucose-treated EPCs, and EPCs from diabetic patients resulting in eNOS-mediated O2− production. Subsequent reduction of EPC levels and impairment of EPC function likely contributes to the pathogenesis of vascular disease in diabetes.
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Cites
Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes
Gæde, P., Vedel, P., Larsen, N., Jensen, G. V. H., Parving, H.-H., & Pedersen, O. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa021778 · Cited by 4,378
Circulating endothelial progenitor cells, vascular function, and cardiovascular risk
Hill, J. M., Zalos, G., Halcox, J. P. J., Schenke, W. H., Waclawiw, M. A., Quyyumi, A. A., & Finkel, T. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa022287 · Cited by 3,423
Circulating endothelial progenitor cells and cardiovascular outcomes
Werner, N., Kosiol, S., Schiegl, T., Ahlers, P., Walenta, K., Link, A., Böhm, M., & Nickenig, G. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa043814 · Cited by 2,048
Endothelial Nitric Oxide Synthase in Vascular Disease: From Marvel to Menace
Förstermann, U., & Münzel, T. (2006) · Circulation · doi:10.1161/circulationaha.105.602532 · Cited by 1,957 · cited 6×
“eNOS uncoupling was shown in a variety of experimental and clinical vascular disease states, especially in diabetes (6,7,33,35).”
BackgroundInfluentialLandmesser, U., Dikalov, S., Price, S. R., McCann, L., Fukai, T., Holland, S. M., Mitch, W. E., & Harrison, D. G. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200314172 · Cited by 1,660
Interactions of Peroxynitrite, Tetrahydrobiopterin, Ascorbic Acid, and Thiols
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Vascular dysfunction in diabetes mellitus
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Alp, N. J., McAteer, M. A., Khoo, J., Choudhury, R. P., & Channon, K. M. (2004) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.0000115637.48689.77 · Cited by 194
Cited by
Rochette, L., Lorin, J., Zeller, M., Guilland, J.-C., Lorgis, L., Cottin, Y., & Vergely, C. (2013) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2013.07.004 · Cited by 456
The Role of Oxidative Stress in the Pathophysiology of Gestational Diabetes Mellitus
Lappas, M., Hiden, U., Desoye, G., Froehlich, J., Mouzon, S. H.-D., & Jawerbaum, A. (2011) · Antioxidants & Redox Signaling · doi:10.1089/ars.2010.3765 · Cited by 442
Sorrentino, S. A., Besler, C., Rohrer, L., Meyer, M., Heinrich, K., Bahlmann, F. H., Mueller, M., Horváth, T., Doerries, C., Heinemann, M., et al. (2010) · Circulation · doi:10.1161/circulationaha.108.836346 · Cited by 402
Aging and disease as modifiers of efficacy of cell therapy
Dimmeler, S., & Leri, A. (2008) · Circulation Research · doi:10.1161/circresaha.108.175943 · Cited by 379
Thomas, S. R., Witting, P. K., & Drummond, G. R. (2008) · Antioxidants & Redox Signaling · doi:10.1089/ars.2008.2027 · Cited by 383
Metadata
- Authors
- Thum, T., Fraccarollo, D., Schultheiss, M., Froese, S., Galuppo, P., Widder, J. D., Tsikas, D., Ertl, G., & Bauersachs, J.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2007-03-01
- Volume
- 56
- Issue
- 3
- Pages
- 666-674
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2101241199
- Cited by
- 410
- References
- 9
- FWCI
- 22.54
- Type
- journal article
- Language
- en
- Open access
- closed
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- Thum, T., Fraccarollo, D., Schultheiss, M., Froese, S., Galuppo, P., Widder, J. D., Tsikas, D., Ertl, G., & Bauersachs, J. (2007). Endothelial Nitric Oxide Synthase Uncoupling Impairs Endothelial Progenitor Cell Mobilization and Function in Diabetes. Diabetes. https://doi.org/10.2337/db06-0699
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