Corgnali, Maddalena, Piconi, Ludovica, Ihnat, Michael and Ceriello, Antonio. (2008) Evaluation of gliclazide ability to attenuate the hyperglycaemic 'memory' induced by high glucose in isolated human endothelial cells. Diabetes - Metabolism: Research and Reviews, Vol.24 (No.4). pp. 301-309. ISSN 1520-7552

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Abstract

Background Patients with long-term exposure to high levels of hyperglycaemia remain more susceptible to diabetes-related complications, even with subsequent lower levels of hyperglycaemia. We sought to confirm the hypothesis that exposure to continuous increased glucose results in a memory of cellular stress in isolated endothelial cells, even when switched back to normal glucose, and to investigate the ability of gliclazide to attenuate this phenomenon. Methods Human umbilical vein endothelial cells were incubated for 21 days in normal glucose (5 mmol/L), high glucose (30 mmol/L), or high glucose for 14 days followed by normal glucose for 7 days (memory condition). The effects of gliclazide (10 mu mol/L) and glibenclamide (1 mu mol/L) were evaluated in the memory condition and added to the culture media early (first 14 days), late (last 7 days), or throughout the study. Oxidative stress and cell apoptosis parameters were investigated. Results Continuous high glucose increased reactive oxygen species, 8-OHdG, nitrotyrosine, caspase-3, and reduced Bcl-2 expression. These deleterious effects were also observed in the memory condition. Gliclazide applied early or throughout the study improved all parameters. In contrast, glibenclamide showed no relevant effect on study parameters. Conclusions Our results suggest that gliclazide prevents endothelial cell apoptosis by reducing oxidative stress. The results appear to confirm the hypothesis that exposure of cells to continuous increased glucose results in a hyperglycaemic cellular memory that remains, even when cells are switched back to normal glucose. Gliclazide attenuated this cellular memory, decreasing oxidative stress and protecting vascular endothelial cells from apoptosis. Copyright (C) 2007 John Wiley & Sons, Ltd.

Item Type:	Journal Article
Subjects:	Q Science > QP Physiology R Medicine > RB Pathology
Divisions:	Faculty of Medicine > Warwick Medical School > Clinical Sciences Research Institute (CSRI) Faculty of Medicine > Warwick Medical School
Library of Congress Subject Headings (LCSH):	Hyperglycemia, Endothelial cells, Oxidative stress, Gliclazide
Journal or Publication Title:	Diabetes - Metabolism: Research and Reviews
Publisher:	John Wiley & Sons Ltd
ISSN:	1520-7552
Date:	May 2008
Volume:	Vol.24
Number:	No.4
Number of Pages:	9
Page Range:	pp. 301-309
Identification Number:	10.1002/dmrr.804
Status:	Peer Reviewed
Publication Status:	Published
Access rights to Published version:	Restricted or Subscription Access
Funder:	Servier Research Institute
References:	1. Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature 2001; 414: 813–820. 2. Cagliero E, Maiello M, Boeri D, Roy S, Lorenzi M. Increased expression of basement membrane components in human endothelial cells cultured in high glucose. J Clin Invest 1988; 82: 735–738. 3. Ihnat MA, Thorpe JE, Kamat CD, et al. Reactive oxygen species mediate a cellular ‘memory’ of high glucose stress signalling. Diabetologia. 2007; 50(7): 1523–1531. 4. Jennings PE, Scott NA, Saniabadi AR, Belch JJF. Effects of gliclazide on platelet reactivity and free radicals in type II diabetic patients: clinical assessment. Metabolism 1992; 41: 36–39. 5. Desfaits AC, Serri O, Renier G. Gliclazide decreases cellmediated low density lipoprotein (LDL) oxidation and reduces monocyte adhesion to endothelial cells induced by oxidatively modified LDL. Metabolism 1997; 46: 1150–1156. 6. Jennings PE, Belch JJF. Free radical scavenging activity of sulfonylureas: a clinical assessment of the effect of gliclazide. Metabolism 2000; 49(S1): 23–26. 7. Jaffe EA, Nachman RL, Becker CG,Minick CR. Culture of human endothelial cells derived from umbilical veins. Identification by morphologic and immunologic criteria. J Clin Invest 1973; 52: 2745–2756. 8. Risso A, Mercuri F, Quagliaro L, Damante G, Ceriello A. Intermittent high glucose enhances apoptosis in human umbilical vein endothelial cells in culture. Am J Physiol 2001; 281: E924–E930. 9. Tesfamariam B. Free radicals in diabetic endothelial dysfunction. Free Radic Biol Med 1994; 16: 383–391. 10. Baynes RW. Role of oxidative stress in development of complications in diabetes. Diabetes 1991; 40: 405–412. 11. Giugliano D, Ceriello A, Paolisso G. Oxidative stress and diabetic vascular complications. Diabetes Care 1998; 19: 257–267. 12. Ceriello A. Effects of gliclazide beyond metabolic control. Metabolism 2006; 55(Suppl. 1): S10–S15. 13. Ceriello A, dello Russo P, Amstad P, Cerutti P. High glucose induces antioxidant enzymes in human endothelial cells in culture. Evidence linking hyperglycemia and oxidative stress. Diabetes 1996; 45: 471–477. 14. Quagliaro L, Piconi L, Assaloni R, Martinellie L, Motz E, Ceriello A. Intermittent high glucose enhances apoptosis related to oxidative stress in human umbilical vein endothelial cells: the role of protein kinase C and NAD(P)H-oxidase activation. Diabetes 2003; 52: 2795–2804. 15. Cagliero E, Roth T, Roy S, Lorenzi M. Characteristics and mechanisms of high-glucose-induced overexpression of basement membrane components in cultured human endothelial cells. Diabetes 1991; 40: 102–110. 16. Mohazzab KM, Kaminski PM, Wolin MS. NADH oxidoreductase is a major source of superoxide anion in bovine coronary artery endothelium. Am J Physiol 1994; 266: H2568–H2572. 17. Rajagopalan S, Kurz S, Munzel T, et al. Angiotensin II-mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NADPH oxidase activation. Contribution to alterations of vasomotor tone. J Clin Invest 1996; 97: 1916–1923. 18. Inoguchi T, Li P, Umeda F, et al. High glucose level and free fatty acid stimulate reactive oxygen species production through protein kinase C-dependant activation of NAD(P)H oxidase in cultured vascular cells. Diabetes 2000; 49: 1939–1945. 19. Koya D, King GL. Protein kinase C activation and the development of diabetic complications. Diabetes 1998; 47: 859–866. 20. Nishikawa T, Edelstein D, Du XL, et al. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature 2000; 404: 787–790. 21. Desfaits AC, Serri O, Renier G. Normalization of plasma lipid peroxides, monocyte adhesion, and tumor necrosis factoralpha production in NIDDM patients after gliclazide treatment. Diabetes Care 1998; 21: 487–493. 22. Fava D, Cassone-Faldetta M, Laurenti O, De Luca O, Ghiselli A, De Mattia G. Gliclazide improves antioxidant status and nitric oxide-mediated vasodilation in Type 2 diabetes. Diabet Med 2002; 19: 752–757. 23. Kimoto K, Kizaki T, Suzuki K, et al. Gliclazide protects pancreatic beta-cells from damage by hydrogen peroxide. Biochem Biophys Res Commun 2003; 303: 112–119. 24. Noda Y, Mori A, Packer L. Gliclazide scavenges hydroxyl, superoxide and nitric oxide radicals: an ESR study. Res Commun Mol Pathol Pharmacol 1997; 96: 115–124. 25. O’Brien RC, Luo M, Balazs N, Mercuri J. In vitro and in vivo antioxidant properties of gliclazide. J Diabetes Complications 2000; 14: 201–206. 26. White NH, Cleary PA, Dahms W, Goldstein D, Malone J, Tamborlane WV, Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and Complications (EDIC) Research Group. Beneficial effects of intensive therapy of diabetes during adolescence: outcomes after the conclusion of the Diabetes Control and Complications Trial (DCCT). J Pediatr 2001; 139: 804–812. 27. Ihnat MA, Thorpe JE, Ceriello A. Hypothesis: the ‘metabolic memory’, the new challenge of diabetes. Diabet Med. 2007; 24(6): 582–586.
URI:	http://wrap.warwick.ac.uk/id/eprint/29921

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