Abstract
Myocardial infarction (MI) is caused by occlusion of coronary artery and insufficient oxygen supply to a certain area of myocardium. Its necrosis appears as a result of MI. The process of tissue repair after MI is very complicated and it is influenced by numerous factors, including growth factors and proteolytic enzymes. The aim of the study was to determine serum transforming growth factor β (TGF-β) concentration on day 2 and 7 after MI and to asses the relationship of this growth factor with serum proteolytic activity of collagenase and elastase. In addition, the effect of fibrynolytic treatment on these factors was evaluated. About 100 patients with MI were enrolled to the study. The control group consisted of 50 healthy individuals. We observed that TGF-β1 concentration correlated positively with collagenase activity on the second day after MI and that it also correlated positively with elastase activity on day 2 and 7 after MI. Moreover, treatment with streptokinase (SK) caused a significant increase of TGF-β serum concentration. Our data indicate that TGF-β1 may be one of the factors involved in tissue repair process after MI. Its effect seems to be mediated by collagenase and elastase and may change with the time that elapsed after MI.
Similar content being viewed by others
References
Ristow, H. J. 1986. BSC-1 growth factor inhibitor/type β transforming growth factor is a strong inhibitor of thymocyte proliferation. Proc. Natl. Acad. Sci. USA. 83:5531–5533.
Blobe, G. C., W. P. Schiemann, and H. F. Lodish. 2000. Role of transforming growth factor β in human disease. N. Engl. J. Med. 342:1350–1358.
Cotran, R. S., V. Kumar, and T. Collins. 1999. Tissue Repair: Cellular Growth, Fibrosis and Wound Healing. W: Robbins pathologic basis of disease, wyd 6, W.B. Saunders Company, Philadelphia, 89–112.
Border, W. A., S. Okuda, L. R. Languino, and E. Ruoslahti. 1990. Transforming growth factor- beta regulates production of proteoglykans by mesangial cells. Kidney. Int. 37:689–693.
Epstein, F. H. 1994. Transforming growth factor beta in tissue fibrosis. N. Eng. J. Med. 19:1286–1294.
Dauterman, K. and T. Chou. 2002. Acute Myocardial Infarction. In: Conn’s Current Therapy 2002, R. E. Rakiel, E. T. Bope ed., W. B. Saunders Company, Philadelphia, 330–331.
Danielpour, D. 1993. Improved sandwich enzyme-linked Immunosorbent Assays for TGFβ1. J. Immunol. Methods 158:17–25.
Shoen, F. J. 1999. The Heart. In: The Pathologic Basis of Disease, 6th edn., R. S. Cotran, V. Kumar, and T. Collins, eds. W. B. Saunders Company, Philadelphia, 543–600.
Sun, Y., J. Q. Zhang, J. Zhang, and S. Lamparter. 2000. Cardiac remodeling by fibrous tissue after infarction in rats. J. Lab. Clin. Med. 135:316–323.
Willems, I. E. M. G., M. G. Havenith, J. G. R. De Mey, and M. J. A. P. Daemen. 1994. The α-smooth muscle actin-positive cells in healing human myocardial scars. Am. J. Pathol. 145:868–875.
Weber, K. T. 1989. Cardiac intrstitium in health and disease: The fibrillar collagen network. J. Am. Coll Cardiol. 13:1637–1652.
Tiggelman, A. M. B. C., C. Linthorst, W. Boers, H. S. Brand, and R. A. F. M. Chamuleau. 1997. Transforming growth factor-beta-induced collagen synthesis by human liver myofibroblasts is inhibited by alpha-2-macroglobulin. J. Hepatol. 26:1220–1228.
Sun, Y., and K. T. Weber. 1996. Angiotensin converting enzyme and myofibroblasts during tissue repair in the rat heart. J. Mol. Cell. Cardiol. 28:851–858.
Desmouliere, A., and G. Gabbiani. 1994. Modulation of fibroblastic cytoskeletal features during pathological situations: The role of extracellular matrix and cytokines. Cell. Motil. Cytoskeleton 29:195–203.
Darby, I., O. Skalli, and G. Gabbiani. 1990. α-smooth muscle actin is transiently expressed by miofibroblast during experimental wound healing. Lab. Invest. 63:21–29.
Ravitz, M. J., and C. E. Wenner. 1997. Cyclin-dependent kinase regulation during G1 phase and cell cycle regulation by TGF-β. Adv. Cancer Res. 71:165–207.
Sanderson, N., V. Factor, P. Nagy, J. Kopp, P. Kondaiah, L. Wakefield, A. B. Roberts, M. B. Sporn, and S. S. Thorgeirsson. 1995. Hepatic expression of mature transforming growth factor beta 1 in transgenic mice results in multiple tissue lesion. Proc. Natl. Acad. Sci. USA. 92:2572–2576.
Rappolee, D. A., D. Mark, M. J. Banda, and Z. Werb. 1988. Wound macrophages express TGF-α and other growth factors in vivo: Analysis by mRNA phenotyping. Science 241:708–712.
Olivetti, G., J. M. Capasso, E. H. Sonnenblick, and P. Anversa. 1990. Side-to-side sllipage of myocytes participates in ventricular wall remodeling acutely after myocardial infarction in rats. Circ. Res. 67:23–28.
Takahashi, S., A. C. Barry, and S. M. Factor. 1990. Collagen degradation in ischaemic rat hearts. Biochem. J. 265:233–241.
Rohde, L. E., A. Ducharme, L. H. Arroyo, M. Aikawa, G. H. Sukhova, A. Lopez-Anaya, K. F. McClure, P. G. Mitchell, P. Libby, and R. T. Lee. 1999. Matrix metalloproteinase inhibition attenuates early left ventricular enlargement after experimental infarction in mice. Circulation 99:3063–3070.
Montfort, I., and R. Perez -Tamyao. 1975. The distribution of collagenase in normal rat tissue. J. Histochem. Cytochem. 23:910–920.
Weiss, S. J. 1989. Tissue destruction by neutrophils. N. Engl. J. Med. 303:365–376.
Jolly, S. R., W. J. Kane, B. G. Hook, G. D. Abrams, S. L. Kunkel, and B. R. Lucchesi. 1986. Reduction of myocardial infarct size by neutrophil depletion: Effect of duration of occlusion. Am. Heart J. 112:682–690.
Lindsey, M. L., J. Gannon, M. Aikawa, F. J. Schoen, E. Rabkin, L. Lopresti-Morrow, J. Crawford, S. Black, P. Libby, P. G. Mitchell, and R. T. Lee. 2002. Selective matrix metalloproteinase inhibition reduces left ventricular remodeling but does not inhibit angiogenesis after myocardial infarction. Circulation 105:753–758.
Ohlsson, K. 1977. The extracellular release of granulocytes collagenase and elastase during phagocytosis and inflammatory process. Scand. J. Hematol. 19:145–161.
Tiefenbacher, C. P., M. Ebert, F. Niroomand, S. Batkai, H. Tillmanns, R. Zimmermann, and W. Kubler. 1997. Inhibition of elastase improves myocardial function after repetitive ischaemia and myocardial infarction in the rat heart. Pflugers Arch. 433:563–570.
Lechleitner, P., J. Mair, N. Genser, F. Dienstl, and B. Puschendorf. 1993. Granulocyte elastase in acute myocardial infarction. Z. Kardiol. 82:641–647.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Czarkowska-P¸czek, B., Przybylski, J., Marciniak, A. et al. Proteolytic Enzymes Activities in Patients After Myocardial Infarction Correlate with Serum Concentration of TGF-β. Inflammation 28, 279–284 (2004). https://doi.org/10.1007/s10753-004-6051-2
Issue Date:
DOI: https://doi.org/10.1007/s10753-004-6051-2