Sobia MUSHTAQ, Tahir ALI, Farhana ALTAF, Muhammad ABDULLAH, İram MURTAZA

Stress-responsive factor regulation in patients suffering from type 2 diabetes and myocardial infarction

Pro-free radical oxidative stresses, as well as regulatory factors, are believed to be the key players in the development of diabetes and heart-related disorders such as myocardial infarction. The aim of the present study was to highlight the role of oxidative stress-responsive factors (reactive oxygen species [ROS], super oxide dismutase [SOD], and calpain-1) in type 2 diabetes and myocardial infarction. Materials and methods: A total of 100 type 2 diabetes patients with myocardial infarction and 50 normal individuals were selected for this analysis. The levels of ROS and activities of SOD in the serum were determined. Serum calpain-1 expression was checked using western blotting. Results: The serum level of ROS and the expression of calpain-1 were significantly higher while the activity of SOD was significantly lower in diabetic patients with myocardial infraction compared to normal individuals. Conclusion: These findings suggest a possible link between decreased antioxidant (SOD) and increased ROS levels as well as calpain-1 expression, supporting the role of oxidative stress-regulatory factors in diabetes and myocardial infraction.

Anahtar Kelimeler:

Diabetes mellitus, myocardial infraction, super oxide dismutase, reactive oxygen species, calpain-1

Stress-responsive factor regulation in patients suffering from type 2 diabetes and myocardial infarction

Keywords:

Diabetes mellitus, myocardial infraction, super oxide dismutase, reactive oxygen species, calpain-1,

PDF

___

Thygesen K, Alpert JS, White HD. Universal definition of myocardial infarction. Eur Heart J 2007; 28: 25–38.
Madsen JK, Thomsen BL, Sİrensen JN. Risk factors and prognosis after discharge for patients admitted because of suspected acute myocardial infarction with and without confirmed diagnosis. Am J Cardiol 1987; 59: 1064–1070.
Herlitz J, Malmberg K, Karlson BW. Mortality and morbidity during a five year follow-up of diabetics with myocardial infarction. Acta Med Scand 1998; 224: 31–38.
Barbas GI, White HD, Modan M. Significance of diabetes mellitus in patients with acute myocardial infarction receiving thrombolytic agents. J Am Coll Cardiol 1993; 22: 707–713.
De Vriese AS, Verbeuren TJ, Van de Voorde J. Endothelial dysfunction in diabetes. Br J Pharmacol 2000; 130: 963–974.
Brawek B, Löffler M, Wagner K, Huppertz H, Wendling A, Weyerbrock A, Jackisch R, Feuerstein T. Reactive oxygen species (ROS) in the human neocortex: Role of aging and cognition. Brain Res Bull 2010; 81: 484–490.
Cave AC, Brewer AC, Narayanapanicker A, Ray R, Grieve DJ, Walker S. NADPH oxidases in cardiovascular health and disease. Antioxid Redox Signal 2006; 8: 691–728.
Ungvári Z, Gupte SA, Recchia FA, Bátkai S, Pacher P. Role of oxidative-nitrosative stress and downstream pathways in various forms of cardiomyopathy and heart failure. Curr Vasc Pharmacol 2005; 3: 221–229.
Valko M, Rhodes CJ, Moncola J, Izakovic M, Mazura M. Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chem Biol Interact 2006; 160: 1–40.
Chen Y, Hou M, Li Y, Traverse J H, Zhang P, Salvemini D. Increased superoxide production causes coronary endothelial dysfunction and depressed oxygen consumption in the failing heart. Am J Physiol Heart Circ Physiol 2005; 288: H133–H141.
Goll DE, Thompson VF, Li H, Wei W, Cong J. The calpain system. Physiol Rev 2003; 83: 731–801.
Lebart MC, Benyamin Y. The calpain system. FEBS J 2006; 273: 3415–3426.
Taneike M, Mizote I, Morita T, Watanabe T, Hikoso S, Yamaguchi O. Calpain protects the heart from hemodynamic stress. J Biol Chem 2011; 286: 32170–32177.
Gurevitch J, Frolkis I, Yuhas Y, Lifschitz-Mercer B, Berger E, Paz Y. Antitumor necrosis factor-alpha improves myocardial recovery after ischemia and reperfusion. J Am Coll Cardiol 1997; 30: 1554–1561.
Gao WD, Atar D, Liu Y, Perez NG, Murphy AM, Marban E. Role of troponin I proteolysis in the pathogenesis of stunned myocardium. Circ Res 1997; 80: 393–399.
Koşar F, Varol E, Ileri M, Ayaz S, Hisar I, Kisacik H. Circulating cytokines and complements in chronic heart failure. Angiology 1999; 50: 403–408.
Wood DE, Newcomb EW. Cleavage of Bax enhances its cell death function. Exp Cell Res 2000; 256: 375–382.
Sorimachi Y, Harada K, Saido TC, Ono T, Kawashima S, Yoshida K. Downregulation of calpastatin in rat heart after brief ischemia and reperfusion. J Biochem 1997; 122: 743–748.
Kakkar R, Wang X, Radhi JM, Rajala RV, Wang R, Sharma RK. Decreased expression of high-molecular-weight calmodulin- binding protein and its correlation with apoptosis in ischemia- reperfused rat heart. Cell Calcium 2001; 29: 59–71.
Chen M, He H, Zhan S, Krajewski S, Reed JC, Gottlieb RA. Bid is cleaved by calpain to an active fragment in vitro and during myocardial ischemia/reperfusion. J Biol Chem 2001; 276: 30724–30728.
Nakagawa T, Yuan J. Cross-talk between two cysteine protease families. Activation of caspase-12 by calpain in apoptosis. J Cell Biol 2000; 150: 887–894.
Hayashi I, Morishita Y, Imai K, Nakamura M, Nakachi K, Hayashi T. High-throughput spectrophotometric assay of reactive oxygen species in serum. Mutat Res 2007; 631: 55–61.
Beyer WF Jr, Fridovich I. Assaying for superoxide dismutase activity: some large consequences of minor changes in conditions. Anal Biochem 1987; 161: 559–566.
Erne P, Radovanovic D, Urban P, Stauffer JC, Berteal O, Gutzwiller F. Early drug therapy and in-hospital mortality following acute myocardial infarction. Heart Drug 2003; 3: 134–140.
Dunn JS, Freed BM, Gustafson DL, Stringer KA. Inhibition of human neutrophil reactive oxygen species production and p67phox translocation by cigarette smoke extract. Atherosclerosis 2005; 179: 261–267.
Ishii H, Suzuki Y, Kuboki M, Morikawa M, Inoue M, Kazama M. Activation of calpain I in thrombin-stimulated platelets is regulated by the initial elevation of the cytosolic Ca2+ concentration. Biochem J 1992; 284: 755–760.
Hood JL, Brooks WH, Roszman TL. Subcellular mobility of the calpain/calpastatin network: an organelle transient. BioEssays 2006; 28: 850–859.
Li Y, Ma J, Zhu H, Singh M, Hill D, Greer PA, Arnold JM, Abel ED, Peng T. Targeted inhibition of calpain reduces myocardial hypertrophy and fibrosis in mouse models of type 1 diabetes. Diabetes 2011; 60: 2985–2994.
Ling C, Groop L, Del Guerra S, Lupi R. Calpain-10 expression is elevated in pancreatic islets from patients with type 2 diabetes. PLoS ONE 2009; 4: e6558.
Sato Y, Kuwajima M, Kamiya H, Harashima H. Calpain 10 as a predictive gene for type 2 diabetes: evidence from a novel screening system using white blood cells of Otsuka Long- Evans Tokushima Fatty (OLETF) rats. Biol Pharm Bull. 2003; 26: 1765–1768.
Levy J, Gavin JR 3rd, Sowers JR. Diabetes mellitus: a disease of abnormal cellular calcium metabolism? Am J Med 1994; 96: 260–273.
Praveen KS, Mahendra S, Lokesh D, Saneesh V, Anjana S, Jeena J, Krupa AM, Godi R, George T, Sreekumar E et al. Calpain and reactive oxygen species targets Bax for mitochondrial permeabilisation and caspase activation in zerumbone induced apoptosis. PLoS ONE 2013; 8: e59350.
Najar RA, Ghaderian SMH, Vakili H, Panah AST, Farimani AR, Rezaie G, Harchegani AB. The role of p53, bax, bcl2, and 8-OHdG in human acute myocardial infarction. Cent Eur J Biol 2010; 5: 439–445.
Gill C, Mestril R, Samali A. Losing heart: the role of apoptosis in heart disease--a novel therapeutic target? FASEB J 2002; 16: 135–146.