Vol 28, No 6 (2021)
Original Article
Published online: 2019-03-26

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Selected matrix metalloproteinases activity and hypertension-mediated organ damage in relation to uric acid serum level

Krystian Gruszka1, Marek Rajzer1, Tomasz Drożdż1, Wiktoria Wojciechowska1, Tomasz Pizoń1, Kamila Migacz-Gruszka2, Danuta Czarnecka1
Pubmed: 30994184
Cardiol J 2021;28(6):905-913.

Abstract

Background: Atherosclerosis is as a systemic inflammatory disease associated with the activationof many mediators, including matrix metalloproteinases (MMPs), and may be amplified by abnormal high serum uric acid (UA) concentration (hyperuricemia, HU). The aim of the study was to determine the relationship between serum UA concentration and activity of MMPs and their correlation with the hypertension-mediated organ damage (HMOD) intensity.
Methods: One hundred and nine patients untreated with antihypertensive, hypolipemic or uratelowering drugs with diagnosed stage 1–2 essential hypertension were included in this study. In all participants blood pressure (BP) was measured, carotid-femoral pulse wave velocity (PWV), intima–media thickness (IMT), echocardiography and blood tests including UA, lipids and serum concentrations of MMPs (1, 2, 3, 9) were observed. The participants were divided into hyper- and normuricemic groups.
Results: Uric acid concentration in the whole study group positively correlated with some HMOD parameters (IMT, PWV, left ventricular mass index, left atrial dimension). Among the studied metalloproteinases only MMP-3 activity positively correlated with serum UA concentration independently of age, body mass index and serum lipids (R2 = 0.11, p = 0.048). Multivariate regression analysis showed positive association between IMT and BP, UA concentration and MMP-3 activity, independently of waist circumference and serum lipids (R2 = 0.328, p < 0.002). Patients with HU were characterized by higher activity of MMP-3 than those without (19.41 [14.45; 21.74] vs. 13.98 [9.52; 18.97] ng/mL, p = 0.016).
Conclusions: The present results may support the thesis that UA and the increased by UA activity of MMPs may take part in the development of HMOD, especially IMT.

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References

  1. Galis ZS, Khatri JJ. Matrix metalloproteinases in vascular remodeling and atherogenesis: the good, the bad, and the ugly. Circ Res. 2002; 90(3): 251–262.
  2. Matsuyama A, Sakai N, Ishigami M, et al. Matrix metalloproteinases as novel disease markers in Takayasu arteritis. Circulation. 2003; 108(12): 1469–1473.
  3. Vitlianova K, Georgieva J, Milanova M, et al. Blood pressure control predicts plasma matrix metalloproteinase-9 in diabetes mellitus type II. Arch Med Sci. 2015; 11(1): 85–91.
  4. Visse R, Nagase H. Matrix metalloproteinases and tissue inhibitors of metalloproteinases: structure, function, and biochemistry. Circ Res. 2003; 92(8): 827–839.
  5. Johnson JL. Matrix metalloproteinases: influence on smooth muscle cells and atherosclerotic plaque stability. Expert Rev Cardiovasc Ther. 2007; 5(2): 265–282.
  6. Johnson J. Metalloproteinases in atherosclerosis. Eur J Pharmacol. 2017; 816: 93–106.
  7. Raffetto J, Khalil R. Matrix metalloproteinases and their inhibitors in vascular remodeling and vascular disease. Biochem Pharmacol. 2008; 75(2): 346–359.
  8. Jaiswal A, Chhabra A, Malhotra U, et al. Comparative analysis of human matrix metalloproteinases: Emerging therapeutic targets in diseases. Bioinformation. 2011; 6(1): 23–30.
  9. Zhu Y, Pandya BJ, Choi HK. Prevalence of gout and hyperuricemia in the US general population: the National Health and Nutrition Examination Survey 2007-2008. Arthritis Rheum. 2011; 63(10): 3136–3141.
  10. Kumar A U A, Browne LD, Li X, et al. Temporal trends in hyperuricaemia in the Irish health system from 2006-2014: A cohort study. PLoS One. 2018; 13(5): e0198197.
  11. Thiele P, Schröder HE. Epidemiology of hyperuricemia and gout. Z Gesamte Inn Med. 1982; 37(13): 406–410.
  12. Abeles AM. Hyperuricemia, gout, and cardiovascular disease: an update. Curr Rheumatol Rep. 2015; 17(3): 13.
  13. Johnson RJ, Kang DH, Feig D, et al. Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease? Hypertension. 2003; 41(6): 1183–1190.
  14. Li M, Hu X, Fan Y, et al. Hyperuricemia and the risk for coronary heart disease morbidity and mortality a systematic review and dose-response meta-analysis. Sci Rep. 2016; 6: 19520.
  15. Qin T, Zhou X, Wang Ji, et al. Hyperuricemia and the Prognosis of Hypertensive Patients: A Systematic Review and Meta-Analysis. J Clin Hypertens (Greenwich). 2016; 18(12): 1268–1278.
  16. Williams B, Mancia G, Spiering W, et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension. J Hypertens. 2018; 36(10): 1953–2041.
  17. Laurent S, Cockcroft J, Bortel LV, et al. Expert consensus document on arterial stiffness: methodological issues and clinical applications. European Heart Journal. 2006; 27(21): 2588–2605.
  18. Van Bortel LM, Laurent S, Boutouyrie P, et al. Expert consensus document on the measurement of aortic stiffness in daily practice using carotid-femoral pulse wave velocity. J Hypertens. 2012; 30(3): 445–448.
  19. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man. Anatomic validation of the method. Circulation. 1977; 55(4): 613–618.
  20. Touboul PJ, Hennerici MG, Meairs S, et al. Mannheim Carotid Intima-Media Thickness and Plaque Consensus (2004–2006–2011). Cerebrovasc Dis. 2012; 34(4): 290–296.
  21. Gunter EW, Lewis BG, Koncikowski SM. Laboratory procedures used for the Third National Health and Nutrition Examination Survey (NHANES III), 1988–1994. U.S. Department Of Health And Human Services. 1996. . https://www.cdc.gov/nchs/data/nhanes/nhanes3/cdrom/nchs/manuals/labman.pdf.
  22. Sundström J, Sullivan L, D'Agostino RB, et al. Relations of serum uric acid to longitudinal blood pressure tracking and hypertension incidence. Hypertension. 2005; 45(1): 28–33.
  23. Silva HA, Carraro JC, Bressan J, et al. Relation between uric acid and metabolic syndrome in subjects with cardiometabolic risk. Einstein (Sao Paulo). 2015; 13(2): 202–208.
  24. Wang H, Zhang H, Sun L, et al. Roles of hyperuricemia in metabolic syndrome and cardiac-kidney-vascular system diseases. Am J Transl Res. 2018; 10(9): 2749–2763.
  25. Alberti KG, Zimmet P, Shaw J. Metabolic syndrome--a new world-wide definition. A Consensus Statement from the International Diabetes Federation. Diabet Med. 2006; 23(5): 469–480.
  26. Woessner JF. Matrix metalloproteinases and their inhibitors in connective tissue remodeling. FASEB J. 1991; 5(8): 2145–2154.
  27. Ye S. Influence of matrix metalloproteinase genotype on cardiovascular disease susceptibility and outcome. Cardiovasc Res. 2006; 69(3): 636–645.
  28. Heagerty AM, Aalkjaer C, Bund SJ, et al. Small artery structure in hypertension. Dual processes of remodeling and growth. Hypertension. 1993; 21(4): 391–397.
  29. Peeters SA, Engelen L, Buijs J, et al. Plasma matrix metalloproteinases are associated with incident cardiovascular disease and all-cause mortality in patients with type 1 diabetes: a 12-year follow-up study. Cardiovasc Diabetol. 2017; 16(1): 55.
  30. Zucker S, Lysik RM, Zarrabi MH, et al. Elevated plasma stromelysin levels in arthritis. J Rheumatol. 1994; 21(12): 2329–2333.
  31. Ribbens C, Martin y Porras M, Franchimont N, et al. Increased matrix metalloproteinase-3 serum levels in rheumatic diseases: relationship with synovitis and steroid treatment. Ann Rheum Dis. 2002; 61(2): 161–166.
  32. Kotajima L, Aotsuka S, Fujimani M, et al. Increased levels of matrix metalloproteinase-3 in sera from patients with active lupus nephritis. Clin Exp Rheumatol. 1998; 16(4): 409–415.
  33. Leyva F. Uric acid in chronic heart failure: a marker of chronic inflammation. Eur Heart J. 1998; 19(12): 1814–1822.
  34. Wingrove CS, Garr ED, Leyva F, et al. Elevated circulating matrix metalloproteinase-2 in coronary heart disease (abstr). Eur Hear J Abstr. 1998; 19(Suppl. ): 613.
  35. Tan C, Liu Yi, Li W, et al. Associations of matrix metalloproteinase-9 and monocyte chemoattractant protein-1 concentrations with carotid atherosclerosis, based on measurements of plaque and intima-media thickness. Atherosclerosis. 2014; 232(1): 199–203.
  36. Wang Y, Guo W, Li Y, et al. Hypothermia induced by adenosine 5'-monophosphate attenuates injury in an L-arginine-induced acute pancreatitis rat model. J Gastroenterol Hepatol. 2014; 29(4): 742–748.
  37. Amaro S, Obach V, Cervera A, et al. Course of matrix metalloproteinase-9 isoforms after the administration of uric acid in patients with acute stroke. J Neurol. 2009; 256(4): 651–656.
  38. Lien LM, Hsieh YC, Bai CH, et al. Association of blood active matrix metalloproteinase-3 with carotid plaque score from a community population in Taiwan. Atherosclerosis. 2010; 212(2): 595–600.
  39. Kawamoto R, Tomita H, Oka Y, et al. Relationship between serum uric acid concentration, metabolic syndrome and carotid atherosclerosis. Intern Med. 2006; 45(9): 605–614.
  40. Li Y, Lu J, Wu X, et al. Serum uric acid concentration and asymptomatic hyperuricemia with subclinical organ damage in general population. Angiology. 2014; 65(7): 634–640.
  41. Mehta T, Nuccio E, McFann K, et al. Association of Uric Acid With Vascular Stiffness in the Framingham Heart Study. Am J Hypertens. 2015; 28(7): 877–883.
  42. Mulè G, Riccobene R, Castiglia A, et al. Relationships between mild hyperuricaemia and aortic stiffness in untreated hypertensive patients. Nutr Metab Cardiovasc Dis. 2014; 24(7): 744–750.
  43. Fang X, Pan C, Chen Y, et al. Assessment of subclinical left ventricular changes in essential hypertensive patients with hyperuricemia: A three-dimensional speckle-tracking echocardiography study. Clin Exp Hypertens. 2017; 39(1): 93–99.
  44. Krishnan E, Hariri A, Dabbous O, et al. Hyperuricemia and the echocardiographic measures of myocardial dysfunction. Congest Heart Fail. 2012; 18(3): 138–143.
  45. Tavil Y, Kaya MG, Oktar SO, et al. Uric acid level and its association with carotid intima-media thickness in patients with hypertension. Atherosclerosis. 2008; 197(1): 159–163.
  46. Sautin YY, Johnson RJ. Uric acid: the oxidant-antioxidant paradox. Nucleosides Nucleotides Nucleic Acids. 2008; 27(6): 608–619.
  47. Pasalic D, Marinkovic N, Feher-Turkovic L. Uric acid as one of the important factors in multifactorial disorders--facts and controversies. Biochem Med (Zagreb). 2012; 22(1): 63–75.
  48. Rajagopalan S, Meng XP, Ramasamy S, et al. Reactive oxygen species produced by macrophage-derived foam cells regulate the activity of vascular matrix metalloproteinases in vitro. Implications for atherosclerotic plaque stability. J Clin Invest. 1996; 98(11): 2572–2579.