The Korean journal of internal medicine

  • 제28권2호
  • /
  • Pages.165-173
  • /
  • 2013
  • /
  • 1226-3303(pISSN)
  • /
  • 2005-6648(eISSN)
대한내과학회 (The Korean Association of Internal Medicine)
권호 표지
DOI QR코드

DOI QR Code

Interleukin-33, matrix metalloproteinase-9, and tissue inhibitor of matrix metalloproteinase-1 in myocardial infarction

  • Guzel, Savas (Department of Biochemistry, Namik Kemal University Faculty of Medicine) ;
  • Serin, Ozden (Department of Biochemistry, Taksim Education and Research Hospital) ;
  • Guzel, Eda Celik (Department of Family Physcian, Namik Kemal University Faculty of Medicine) ;
  • Buyuk, Banu (Department of Internal Medicine, Taksim Training and Research Hospital) ;
  • Yilmaz, Guzin (Department of Biochemistry, Diyarbakir State Hospital) ;
  • Guvenen, Guvenc (Department of Biochemistry, Istanbul Education and Research Hospital)
  • 발행 : 2013.03.01
⟨ 이전 논문 다음 논문 ⟩

초록

Background/Aims: Acute coronary syndrome (ACS) is characterized by increased inflammatory processes and endothelial activation. We investigated the association between ACS and inflammatory mediators and matrix-degrading enzymes. Methods: We prospectively enrolled 55 consecutive patients with ACS: 25 with unstable angina (UA) and 30 with non-ST elevated myocardial infarction (NSTEMI). For comparison, 25 age- and sex-matched subjects with no significant coronary artery stenosis were included as the control group. Peripheral serum levels of interleukin (IL)-33, matrix metalloproteinase (MMP)-9, tissue inhibitor of MMP-1, and C-reactive protein (CRP) were measured on admission, and at 12, 24, 48, and 72 hours after the initial evaluation. Results: Compared to serum levels in the control group, serum levels of IL-33 decreased in the NSTEMI group (p < 0.05), and levels of MMP-9 and tissue inhibitor of matrix metalloproteinase (TIMP)-1 increased in the UA group (p < 0.01, p < 0.05, respectively) and NSTEMI group (p < 0.05, p < 0.05, respectively). IL-33 levels were significantly lower on admission than at 12 hours after the initial evaluation (p < 0.05). IL-33 levels were negatively correlated with MMP-9 levels (r = -0.461, p < 0.05) and CRP levels (r = -0.441, p < 0.05). Conclusions: Elevated levels of MMP-9, TIMP-1, and decreased levels of IL-33 play a role in the development and progression of ACS.

키워드

참고문헌

  1. Ross R. Atherosclerosis: an inf lammatory disease. N Engl J Med 1999;340:115-126. https://doi.org/10.1056/NEJM199901143400207
  2. Libby P. Inf lammation and cardiovascular disease mechanisms. Am J Clin Nutr 2006;83:456S-460S. https://doi.org/10.1093/ajcn/83.2.456S
  3. Li JJ. Inflammation: an important mechanism for different clinical entities of coronary artery diseases. Chin Med J (Engl) 2005;118:1817-1826.
  4. Myllarniemi M, Calderon L, Lemstrom K, Buchdunger E, Hayry P. Inhibition of platelet-derived growth factor receptor tyrosine kinase inhibits vascular smooth muscle cell migration and proliferation. FASEB J 1997;11:1119-1126. https://doi.org/10.1096/fasebj.11.13.9367346
  5. Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation 2002;105:1135-1143. https://doi.org/10.1161/hc0902.104353
  6. Brauer PR. MMPs: role in cardiovascular development and disease. Front Biosci 2006;11:447-478. https://doi.org/10.2741/1810
  7. Schonbeck U, Libby P. CD40 signaling and plaque instability. Circ Res 2001;89:1092-1103. https://doi.org/10.1161/hh2401.101272
  8. Uzui H, Harpf A, Liu M, et al. Increased expression of membrane type 3-matrix metalloproteinase in human atherosclerotic plaque: role of activated macrophages and inf lammatory cytokines. Circulation 2002;106:3024-3030. https://doi.org/10.1161/01.CIR.0000041433.94868.12
  9. Lacraz S, Nicod L, Galve-de Rochemonteix B, Baumberger C, Dayer JM, Welgus HG. Suppression of metalloproteinase biosynthesis in human alveolar macrophages by interleukin-4. J Clin Invest 1992;90:382-388. https://doi.org/10.1172/JCI115872
  10. Lijnen HR. Metalloproteinases in development and progression of vascular disease. Pathophysiol Haemost Thromb 2003;33:275-281. https://doi.org/10.1159/000083814
  11. Hirohata S, Kusachi S, Murakami M, et al. Time dependent alterations of serum matrix metalloproteinase-1 and metalloproteinase-1 tissue inhibitor after successful reperfusion of acute myocardial infarction. Heart 1997;78:278-284. https://doi.org/10.1136/hrt.78.3.278
  12. Kai H, Ikeda H, Yasukawa H, et al. Peripheral blood levels of matrix metalloproteases-2 and -9 are elevated in patients with acute coronary syndromes. J Am Coll Cardiol 1998;32:368-372. https://doi.org/10.1016/S0735-1097(98)00250-2
  13. Etoh T, Joffs C, Deschamps AM, et al. Myocardial and interstitial matrix metalloproteinase activity after acute myocardial infarction in pigs. Am J Physiol Heart Circ Physiol 2001;281:H987-H994. https://doi.org/10.1152/ajpheart.2001.281.3.H987
  14. Creemers EE, Cleutjens JP, Smits JF, Daemen MJ. Matrix metalloproteinase inhibition after myocardial infarction: a new approach to prevent heart failure? Circ Res 2001;89:201-210. https://doi.org/10.1161/hh1501.094396
  15. Dinh W, Futh R, Scheffold T, et al. Increased serum levels of tissue inhibitor of metalloproteinase-1 in patients with acute myocardial infarction. Int Heart J 2009;50:421-431. https://doi.org/10.1536/ihj.50.421
  16. Schmitz J, Owyang A, Oldham E, et al. IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptorrelated protein ST2 and induces T helper type 2-associated cytokines. Immunity 2005;23:479-490. https://doi.org/10.1016/j.immuni.2005.09.015
  17. Bartunek J, Delrue L, Van Durme F, et al. Nonmyocardial production of ST2 protein in human hypertrophy and failure is related to diastolic load. J Am Coll Cardiol 2008;52:2166-2174. https://doi.org/10.1016/j.jacc.2008.09.027
  18. Kuchler AM, Pollheimer J, Balogh J, et al. Nuclear interleukin-33 is generally expressed in resting endothelium but rapidly lost upon angiogenic or proinf lammatory activation. Am J Pathol 2008;173:1229-1242. https://doi.org/10.2353/ajpath.2008.080014
  19. Sanada S, Hakuno D, Higgins LJ, Schreiter ER, McKenzie AN, Lee RT. IL-33 and ST2 comprise a critical biomechanically induced and cardioprotective signaling system. J Clin Invest 2007;117:1538-1549. https://doi.org/10.1172/JCI30634
  20. Miller AM, Xu D, Asquith DL, et al. IL-33 reduces the development of atherosclerosis. J Exp Med 2008;205:339-346. https://doi.org/10.1084/jem.20071868
  21. Daugherty A, Rateri DL. T lymphocytes in atherosclerosis: the yin-yang of Th1 and Th2 influence on lesion formation. Circ Res 2002;90:1039-1040. https://doi.org/10.1161/01.RES.0000021397.28936.F9
  22. Laurat E, Poirier B, Tupin E, et al. In vivo downregulation of T helper cell 1 immune responses reduces atherogenesis in apolipoprotein E-knockout mice. Circulation 2001;104:197-202. https://doi.org/10.1161/01.CIR.104.2.197
  23. Pinderski LJ, Fischbein MP, Subbanagounder G, et al. Overexpression of interleukin-10 by activated T lymphocytes inhibits atherosclerosis in LDL receptordeficient mice by altering lymphocyte and macrophage phenotypes. Circ Res 2002;90:1064-1071. https://doi.org/10.1161/01.RES.0000018941.10726.FA
  24. Hamm CW, Bassand JP, Agewall S, et al. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: the Task Force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2011;32:2999-3054. https://doi.org/10.1093/eurheartj/ehr236
  25. Shah PK, Falk E, Badimon JJ, et al. Human monocytederived macrophages induce collagen breakdown in fibrous caps of atherosclerotic plaques: potential role of matrix-degrading metalloproteinases and implications for plaque rupture. Circulation 1995;92:1565-1569.
  26. Kim SH, Kang YJ, Kim WJ, et al. TWEAK can induce pro-inf lammatory cytokines and matrix metalloproteinase-9 in macrophages. Circ J 2004;68:396-399. https://doi.org/10.1253/circj.68.396
  27. Kalela A, Koivu TA, Sisto T, et al. Serum matrix metalloproteinase-9 concentration in angiographically assessed coronary artery disease. Scand J Clin Lab Invest 2002;62:337-342. https://doi.org/10.1080/00365510260296483
  28. Kaden JJ, Dempf le CE, Sueselbeck T, et al. Time-dependent changes in the plasma concentration of matrix metalloproteinase 9 after acute myocardial infarction. Cardiology 2003;99:140-144. https://doi.org/10.1159/000070670
  29. Higo S, Uematsu M, Yamagishi M, et al. Elevation of plasma matrix metalloproteinase-9 in the culprit coronary artery in patients with acute myocardial infarction: clinical evidence from distal protection. Circ J 2005;69:1180-1185. https://doi.org/10.1253/circj.69.1180
  30. Romanic AM, Burns-Kurtis CL, Gout B, Berrebi-Bertrand I, Ohlstein EH. Matrix metalloproteinase expression in cardiac myocytes following myocardial infarction in the rabbit. Life Sci 2001;68:799-814. https://doi.org/10.1016/S0024-3205(00)00982-6
  31. Kameda K, Matsunaga T, Abe N, et al. Increased pericardial fluid level of matrix metalloproteinase-9 activity in patients with acute myocardial infarction: possible role in the development of cardiac rupture. Circ J 2006;70:673-678. https://doi.org/10.1253/circj.70.673
  32. van den Borne SW, Cleutjens JP, Hanemaaijer R, et al. Increased matrix metalloproteinase-8 and -9 activity in patients with infarct rupture after myocardial infarction. Cardiovasc Pathol 2009;18:37-43. https://doi.org/10.1016/j.carpath.2007.12.012
  33. Inokubo Y, Hanada H, Ishizaka H, Fukushi T, Kamada T, Okumura K. Plasma levels of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 are increased in the coronary circulation in patients with acute coronary syndrome. Am Heart J 2001;141:211-217. https://doi.org/10.1067/mhj.2001.112238
  34. Tziakas DN, Chalikias GK, Hatzinikolaou EI, et al. Nterminal pro-B-type natriuretic peptide and matrix metalloproteinases in early and late left ventricular remodeling after acute myocardial infarction. Am J Cardiol 2005;96:31-34.
  35. Nanni S, Melandri G, Hanemaaijer R, et al. Matrix metalloproteinases in premature coronary atherosclerosis: inf luence of inhibitors, inf lammation, and genetic polymorphisms. Transl Res 2007;149:137-144. https://doi.org/10.1016/j.trsl.2006.09.001
  36. Tan J, Hua Q, Gao J, Fan ZX. Clinical implications of elevated serum interleukin-6, soluble CD40 ligand, metalloproteinase-9, and tissue inhibitor of metalloproteinase-1 in patients with acute ST-segment elevation myocardial infarction. Clin Cardiol 2008;31:413-418. https://doi.org/10.1002/clc.20254
  37. Weinberg EO, Shimpo M, De Keulenaer GW, et al. Expression and regulation of ST2, an interleukin-1 receptor family member, in cardiomyocytes and myocardial infarction. Circulation 2002;106:2961-2966. https://doi.org/10.1161/01.CIR.0000038705.69871.D9
  38. McLaren JE, Michael DR, Salter RC, et al. IL-33 reduces macrophage foam cell formation. J Immunol 2010;185:1222-1229. https://doi.org/10.4049/jimmunol.1000520
  39. Mehta JL, Saldeen TG, Rand K. Interactive role of infection, inf lammation and traditional risk factors in atherosclerosis and coronary artery disease. J Am Coll Cardiol 1998;31:1217-1225. https://doi.org/10.1016/S0735-1097(98)00093-X
  40. Shishehbor MH, Bhatt DL. Inflammation and atherosclerosis. Curr Atheroscler Rep 2004;6:131-139. https://doi.org/10.1007/s11883-004-0102-x

피인용 문헌

  1. Novel inflammatory biomarkers in acute coronary syndrome vol.28, pp.2, 2013, https://doi.org/10.3904/kjim.2013.28.2.156
  2. A Novel Cardiac Bio-Marker: ST2: A Review vol.18, pp.12, 2013, https://doi.org/10.3390/molecules181215314
  3. Actual position of interleukin(IL)-33 in atherosclerosis and heart failure: Great Expectations or En attendant Godot? vol.30, pp.5, 2013, https://doi.org/10.1177/0267659114562269
  4. Markers of increased atherosclerotic risk in patients with chronic kidney disease: a preliminary study vol.15, pp.None, 2013, https://doi.org/10.1186/s12944-016-0191-x
  5. Serum MMP-9 Diagnostics, Prognostics, and Activation in Acute Coronary Syndrome and Its Recurrence vol.11, pp.3, 2013, https://doi.org/10.1007/s12265-018-9789-x
  6. Antibody Microarray Analysis of Plasma Proteins for the Prediction of Histologic Chorioamnionitis in Women With Preterm Premature Rupture of Membranes vol.26, pp.11, 2019, https://doi.org/10.1177/1933719119828043
  7. Predictors of myocardial fibrosis and loss of epicardial adipose tissue volume in the long-term period after myocardial infarction vol.25, pp.2, 2013, https://doi.org/10.15829/1560-4071-2020-2-3474
  8. Expression level and diagnostic value of exosomal NEAT1 / MIR ‐204/ MMP ‐9 in acute ST ‐segment elevation myocardial in vol.72, pp.11, 2013, https://doi.org/10.1002/iub.2376
  9. Identification of biomarker panels as predictors of severity in coronary artery disease vol.25, pp.3, 2013, https://doi.org/10.1111/jcmm.16244