Phosphodiesterase III Inhibition Increases cAMP levels and augments the infarct size limiting effect of a dpp-4 inhibitor in mice with type-2 diabetes mellitus

Cardiovascular Drugs and Therapy

Volumn 26, Issue 6, 2012, Pages 445-456

  Birnbaum, Yochai ^a,b,c   Castillo, Alexander C ^a   Qian, Jinqiao ^d   Ling, Shukuan ^a   Ye, Hongmei ^e   Perez Polo, Jose R ^a   Bajaj, Mandeep ^b   Ye, Yumei ^a  

^a University of Texas Medical Branch School of Medicine   (United States)

^b BAYLOR COLLEGE OF MEDICINE   (United States)

^c TEXAS HEART INSTITUTE   (United States)

^d KUNMING MEDICAL UNIVERSITY   (China)

^e China Astronaut Research and Training Center   (China)

Author keywords

CAMP protein kinase A; Diabetes mellitus; Dipeptidyl peptidase 4; Infarct size; Ischemia; Phosphodiesterase III inhibitor; PTEN; Reperfusion

Indexed keywords

ARACHIDONATE 5 LIPOXYGENASE; CILOSTAZOL; CYCLIC AMP; CYCLIC AMP DEPENDENT PROTEIN KINASE; CYCLIC AMP RESPONSIVE ELEMENT BINDING PROTEIN; DIPEPTIDYL PEPTIDASE IV INHIBITOR; ENDOTHELIAL NITRIC OXIDE SYNTHASE; MK 0626; PHOSPHATIDYLINOSITOL 3,4,5 TRISPHOSPHATE 3 PHOSPHATASE; PHOSPHODIESTERASE III; PROTEIN KINASE B; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CONTROLLED STUDY; CORONARY REPERFUSION; DOSE RESPONSE; DRUG EFFECT; DRUG MECHANISM; ENZYME ACTIVITY; ENZYME INHIBITION; HEART INFARCTION; HEART INFARCTION SIZE; HEART PROTECTION; HYPERTENSION; MALE; MOUSE; NON INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; PRIORITY JOURNAL;

ANIMALS; BLOOD GLUCOSE; CYCLIC AMP; CYCLIC AMP-DEPENDENT PROTEIN KINASES; DIABETES MELLITUS, TYPE 2; DISEASE MODELS, ANIMAL; DOSE-RESPONSE RELATIONSHIP, DRUG; DRUG THERAPY, COMBINATION; GLUCAGON-LIKE PEPTIDE 1; HEMOGLOBIN A, GLYCOSYLATED; IMMUNOBLOTTING; LIPIDS; LIPOXINS; MALE; MEMBRANE PROTEINS; MICE; MYOCARDIAL INFARCTION; MYOCARDIUM; PHOSPHODIESTERASE 3 INHIBITORS; PTEN PHOSPHOHYDROLASE; TETRAZOLES; TRIAZOLES;

EID: 84871003029     PISSN: 09203206     EISSN: 15737241     Source Type: Journal    
DOI: 10.1007/s10557-012-6409-x     Document Type: Article

References (58)

1. Yazbeck R, Howarth GS, Abbott CA. Dipeptidyl peptidase inhibitors, an emerging drug class for inflammatory disease? Trends Pharmacol Sci. 2009;30:600-7.
2. Jose T, Inzucchi SE. Cardiovascular effects of the DPP-4 inhibitors. Diab Vasc Dis Res. 2012;9:109-16.
3. Gorrell MD. Dipeptidyl peptidase IV and related enzymes in cell biology and liver disorders. Clin Sci (Lond). 2005;108:277-92.
4. Holst JJ. The physiology of glucagon-like peptide 1. Physiol Rev. 2007;87:1409-39.
5. Lee JG, Kang DG, Yu Jr., Kim Y, Kim J, Koh G, et al. Changes in adenosine deaminase activity in patients with type 2 diabetes mellitus and effect of DPP-4 inhibitor treatment on ADA activity. Diabetes Metab J. 2011;35:149-58.
6. Ye Y, Perez-Polo Jr., Aguilar D, Birnbaum Y. The potential effects of anti-diabetic medications on myocardial ischemia-reperfusion injury. Basic Res Cardiol. 2011;106:925-52.
7. Lonborg J, Vejlstrup N, Kelbaek H, Botker HE, KimWY,Mathiasen AB et al. Exenatide reduces reperfusion injury in patients with STsegment elevation myocardial infarction. Eur Heart J. 2011.
8. Chinda K, Chattipakorn S, Chattipakorn N. Cardioprotective effects of incretin during ischaemia-reperfusion. Diab Vasc Dis Res. 2012
9. Ye Y, Keyes KT, Zhang C, Perez-Polo Jr., Lin Y, Birnbaum Y. The myocardial infarct size-limiting effect of sitagliptin is PKAdependent, whereas the protective effect of pioglitazone is partially dependent on PKA. Am J Physiol Heart Circ Physiol. 2010;298: H1454-65.
10. Huisamen B, Genis A, Marais E, Lochner A. Pre-treatment with a DPP-4 inhibitor is infarct sparing in hearts from obese, pre-diabetic rats. Cardiovasc Drugs Ther. 2011;25:13-20.
11. Chinda K, Palee S, Surinkaew S, Phornphutkul M, Chattipakorn S, Chattipakorn N. Cardioprotective effect of dipeptidyl peptidase- 4 inhibitor during ischemia-reperfusion injury. Int J Cardiol. 2012
12. Yin M, Sillje HH, Meissner M, van Gilst WH, de Boer RA. Early and late effects of the DPP-4 inhibitor vildagliptin in a rat model of post-myocardial infarction heart failure. Cardiovasc Diabetol. 2011;10:85.
13. Doyle ME, Egan JM. Mechanisms of action of glucagon-like peptide 1 in the pancreas. Pharmacol Ther. 2007;113:546-93.
14. Sanada S, Asanuma H, Tsukamoto O, Minamino T, Node K, Takashima S, et al. Protein kinase A as another mediator of ischemic preconditioning independent of protein kinase C. Circulation. 2004;110:51-7.
15. Kambayashi J, Liu Y, Sun B, Shakur Y, Yoshitake M, Czerwiec F. Cilostazol as a unique antithrombotic agent. Curr Pharm Des. 2003;9:2289-302.
16. Liu Y, Fong M, Cone J, Wang S, Yoshitake M, Kambayashi J. Inhibition of adenosine uptake and augmentation of ischemiainduced increase of interstitial adenosine by cilostazol, an agent to treat intermittent claudication. J Cardiovasc Pharmacol. 2000;36:351-60.
17. Manickavasagam S, Ye Y, Lin Y, Perez-Polo RJ, Huang MH, Lui CY, et al. The cardioprotective effect of a statin and cilostazol combination: relationship to Akt and endothelial nitric oxide synthase activation. Cardiovasc Drugs Ther. 2007;21:321-30.
18. Birnbaum Y, Castillo AC, Ling S, Bajaj M, Perez-Polo Jr., Ye Y. Amplification of the myocardial infarct size limiting effects of exenatide with cilostazol, a phosphodiesterase III inhibitor [Abstract]. J Am Col Cardiol. 2012;59:A110.
19. Ye Y, Lin Y, Perez-Polo Jr., Uretsky BF, Ye Z, Tieu BC, et al. Phosphorylation of 5-lipoxygenase at ser523 by protein kinase A determines whether pioglitazone and atorvastatin induce proinflammatory leukotriene B4 or anti-inflammatory 15-epi-lipoxin a4 production. J Immunol. 2008;181:3515-23.
20. Mocanu MM, Field DC, Yellon DM. A potential role for PTEN in the diabetic heart. Cardiovasc Drugs Ther. 2006;20:319-21.
21. Tsang A, Hausenloy DJ, Mocanu MM, Carr RD, Yellon DM. Preconditioning the diabetic heart: the importance of Akt phosphorylation. Diabetes. 2005;54:2360-4.
22. Keyes KT, Xu J, Long B, Zhang C, Hu Z, Ye Y. Pharmacological inhibition of PTEN limits myocardial infarct size and improves left ventricular function postinfarction. Am J Physiol Heart Circ Physiol. 2010;298:H1198-208.
23. Hong KW, Kim KY, Shin HK, Lee JH, Choi JM, Kwak YG, et al. Cilostazol prevents tumor necrosis factor-alpha-induced cell death by suppression of phosphatase and tensin homolog deleted from chromosome 10 phosphorylation and activation of Akt/cyclic AMP response element-binding protein phosphorylation. J Pharmacol Exp Ther. 2003;306:1182-90.
24. Kim KY, Shin HK, Lee JH, Kim CD, Lee WS, Rhim BY, et al. Cilostazol enhances casein kinase 2 phosphorylation and suppresses tumor necrosis factor-alpha-induced increased phosphatase and tensin homolog deleted from chromosome 10 phosphorylation and apoptotic cell death in SK-N-SH cells. J Pharmacol Exp Ther. 2004;308:97-104.
25. Lee JH, Park SY, Lee WS, Hong KW. Lack of antiapoptotic effects of antiplatelet drug, aspirin and clopidogrel, and antioxidant, MCI- 186, against focal ischemic brain damage in rats. Neurol Res. 2005;27:483-92.
26. Ye Y, Qian J, Castillo AC, Perez-Polo Jr., Birnbaum Y. Aliskiren and valsartan reduce myocardial AT1 receptor expression and limit myocardial infarct size in diabetic mice. Cardiovasc Drugs Ther. 2011;25:505-15.
27. Park SY, Lee JH, Kim KY, Kim EK, Yun SJ, Kim CD, et al. Cilostazol increases 3T3-L1 preadipocyte differentiation with improved glucose uptake associated with activation of peroxisome proliferator-activated receptor-gamma transcription. Atherosclerosis. 2008;201:258-65.
28. Nakaya Y,Minami A, Sakamoto S, Niwa Y, OhnakaM, Harada N, et al. Cilostazol, a phosphodiesterase inhibitor, improves insulin sensitivity in the Otsuka Long-Evans Tokushima Fatty Rat, a model of spontaneous NIDDM. Diabetes Obes Metab. 1999;1:37-41.
29. Park SY, Shin HK, Lee JH, Kim CD, Lee WS, Rhim BY, et al. Cilostazol ameliorates metabolic abnormalities with suppression of proinflammatory markers in a db/db mouse model of type 2 diabetes via activation of peroxisome proliferatoractivated receptor gamma transcription. J Pharmacol Exp Ther. 2009;329:571-9.
30. Shen YH, Zhang L, Gan Y, Wang X, Wang J, LeMaire SA, et al. Up-regulation of PTEN (phosphatase and tensin homolog deleted on chromosome ten) mediates p38 MAPK stress signal-induced inhibition of insulin signaling. A cross-talk between stress signaling and insulin signaling in resistin-treated human endothelial cells. J Biol Chem. 2006;281:7727-36.
31. Tani T, Uehara K, Sudo T, Marukawa K, Yasuda Y, Kimura Y. Cilostazol, a selective type III phosphodiesterase inhibitor, decreases triglyceride and increases HDL cholesterol levels by increasing lipoprotein lipase activity in rats. Atherosclerosis. 2000;152:299-305.
32. O'Donnell ME, Badger SA, Sharif MA, Makar RR, Young IS, Lee B, et al. The vascular and biochemical effects of cilostazol in diabetic patients with peripheral arterial disease. Vasc Endovascular Surg. 2009;43:132-43.
33. Smith JA. Measuring treatment effects of cilostazol on clinical trial endpoints in patients with intermittent claudication. Clin Cardiol. 2002;25:91-4.
34. Feliciello A, Gottesman ME, Avvedimento EV. cAMP-PKA signaling to the mitochondria: protein scaffolds, mRNA and phosphatases. Cell Signal. 2005;17:279-87.
35. Inserte J, Garcia-Dorado D, Ruiz-Meana M, Agullo L, Pina P, Soler-Soler J. Ischemic preconditioning attenuates calpainmediated degradation of structural proteins through a protein kinase A-dependent mechanism. Cardiovasc Res. 2004;64:105-14.
36. Sanada S, Kitakaze M, Papst PJ, Asanuma H, Node K, Takashima S, et al. Cardioprotective effect afforded by transient exposure to phosphodiesterase III inhibitors: the role of protein kinase A and p38 mitogen-activated protein kinase. Circulation. 2001;104:705-10.
37. Vadas O, Burke JE, Zhang X, Berndt A, Williams RL. Structural basis for activation and inhibition of class I phosphoinositide 3- kinases. Sci Signal. 2011;4:re2.
38. Cosentino C, Di Domenico M, Porcellini A, Cuozzo C, De Gregorio G, Santillo MR, et al. p85 regulatory subunit of PI3K mediates cAMP-PKA and estrogens biological effects on growth and survival. Oncogene. 2007;26:2095-103.
39. De Gregorio G, Coppa A, Cosentino C, Ucci S, Messina S, Nicolussi A, et al. The p85 regulatory subunit of PI3K mediates TSH-cAMP-PKA growth and survival signals. Oncogene. 2007;26:2039-47.
40. Bellis A, Castaldo D, Trimarco V,MontiMG, Chivasso P, Sadoshima J, et al. Cross-talk between PKA and Akt protects endothelial cells from apoptosis in the late ischemic preconditioning. Arterioscler Thromb Vasc Biol. 2009;29:1207-12.
41. Oudit GY, Penninger JM. Cardiac regulation by phosphoinositide 3-kinases and PTEN. Cardiovasc Res. 2009;82:250-60.
42. Ross AH, Gericke A. Phosphorylation keeps PTEN phosphatase closed for business. Proc Natl Acad Sci U S A. 2009;106:1297-8.
43. Hausenloy DJ, Yellon DM. Survival kinases in ischemic preconditioning and postconditioning. Cardiovasc Res. 2006;70:240-53.
44. Harris MB, Blackstone MA, Sood SG, Li C, Goolsby JM, Venema VJ, et al. Acute activation and phosphorylation of endothelial nitric oxide synthase by HMG-CoA reductase inhibitors. Am J Physiol Heart Circ Physiol. 2004;287:H560-6.
45. Qian J, Ling S, Castillo AC, Long B, Birnbaum Y, Ye Y. Regulation of phosphatase and tensin homolog on chromosome 10 in response to hypoxia. Am J Physiol Heart Circ Physiol. 2012;302: H1806-17.
46. Lee JH, Kim KY, Lee YK, Park SY, Kim CD, Lee WS, et al. Cilostazol prevents focal cerebral ischemic injury by enhancing casein kinase 2 phosphorylation and suppression of phosphatase and tensin homolog deleted from chromosome 10 phosphorylation in rats. J Pharmacol Exp Ther. 2004;308:896-903.
47. Shaywitz AJ, Greenberg ME. CREB: a stimulus-induced transcription factor activated by a diverse array of extracellular signals. Annu Rev Biochem. 1999;68:821-61.
48. Marais E, Genade S, Lochner A. CREB activation and ischaemic preconditioning. Cardiovasc Drugs Ther. 2008;22:3-17.
49. Nagy N, Shiroto K, Malik G, Huang CK, Gaestel M, Abdellatif M, et al. Ischemic preconditioning involves dual cardio-protective axes with p38MAPK as upstream target. J Mol Cell Cardiol. 2007;42:981-90.
50. Das S, Cordis GA, Maulik N, Das DK. Pharmacological preconditioning with resveratrol: role of CREB-dependent Bcl-2 signaling via adenosine A3 receptor activation. Am J Physiol Heart Circ Physiol. 2005;288:H328-35.
51. Eliseev RA, Vanwinkle B, Rosier RN, Gunter TE. Diazoxidemediated preconditioning against apoptosis involves activation of cAMP-response element-binding protein (CREB) and NFkappaB. J Biol Chem. 2004;279:46748-54.
52. Hong KW, Lee JH, Kima KY, Park SY, Lee WS. Cilostazol: therapeutic potential against focal cerebral ischemic damage. Curr Pharm Des. 2006;12:565-73.
53. Gu T, Zhang Z, Wang J, Guo J, Shen WH, Yin Y. CREB is a novel nuclear target of PTEN phosphatase. Cancer Res. 2011;71:2821-5.
54. Timmers L, Henriques JP, de Kleijn DP, Devries JH, Kemperman H, Steendijk P, et al. Exenatide reduces infarct size and improves cardiac function in a porcine model of ischemia and reperfusion injury. J Am Coll Cardiol. 2009;53:501-10.
55. Ban K, Kim KH, Cho CK, Sauve M, Diamandis EP, Backx PH, et al. Glucagon-like peptide (GLP)-1(9-36)amide-mediated cytoprotection is blocked by exendin(9-39) yet does not require the known GLP-1 receptor. Endocrinology. 2010;151:1520-31.
56. Bose AK, Mocanu MM, Carr RD, Brand CL, Yellon DM. Glucagon-like peptide 1 can directly protect the heart against ischemia/reperfusion injury. Diabetes. 2005;54:146-51.
57. Birnbaum Y, Ye Y, Lin Y, Freeberg SY, Nishi SP, Martinez JD, et al. Augmentation of myocardial production of 15-epi-lipoxin-a4 by pioglitazone and atorvastatin in the rat. Circulation. 2006;114:929-35.
58. Keyes KT, Ye Y, Lin Y, Zhang C, Perez-Polo Jr., Gjorstrup P, et al. Resolvin E1 protects the rat heart against reperfusion injury. Am J Physiol Heart Circ Physiol. 2010;299:H153-64.