Der akute Myokardinfarkt gefolgt von einem linksventrikulären Remodellingprozess ist eine der Hauptursachen für die chronische Herzinsuffizienz in der westlichen Welt. Basierend auf der Hypothese, dass apoptotische Zellen einen protektiven Effekt im Szenario eines Herzinfarkts aufweisen könnten, testeten wir diesen Mechanismus experimentell im Klein- und im klinisch relevanteren Großtiermodell. Im Speziellen zeigten parakrine Faktoren, die während des Apoptoseprozesses von Leukozyten sezerniert wurden, ein großes therapeutisches Potential, das vielfältige Vorteile gegenüber der bisher bekannten Stammzellentherapie bieten könnte.
Literatur
Velagaleti RS, Pencina MJ, Murabito JM et al.: Long-term trends in the incidence of heart failure after myocardial infarction. Circulation. Nov 11 118(20), 2057–62 (2008)
Orlic D, Kajstura J, Chimenti S et al.: Mobilized bone marrow cells repair the infarcted heart, improving function and survival. Proc Natl Acad Sci U S A. Aug 28 98(18), 10344–9 (2001)
Meyer GP, Wollert KC, Lotz J et al.: Intracoronary bone marrow cell transfer after myocardial infarction: 5-year follow-up from the randomized- controlled BOOST trial. Eur Heart J. Dec 30(24), 2978–84 (2009)
Lunde K, Solheim S, Aakhus S et al.: Intracoronary injection of mononuclear bone marrow cells in acute myocardial infarction. N Engl J Med. Sep 21 355(12), 1199–209 (2006)
Thum T, Bauersachs J, Poole-Wilson PA et al.: The dying stem cell hypothesis: immune modulation as a novel mechanism for progenitor cell therapy in cardiac muscle. J Am Coll Cardiol. Nov 15 46(10), 1799–802 (2005)
Hoffmann PR, Kench JA, Vondracek A et al.: Interaction between phosphatidylserine and the phosphatidylserine receptor inhibits immune responses in vivo. J Immunol. Feb 1 174(3), 1393–404 (2005)
Ankersmit HJ, Hoetzenecker K, Dietl W et al. Irradiated cultured apoptotic peripheral blood mononuclear cells regenerate infarcted myocardium. Eur J Clin Invest. 2009 Jun;39(6):445–56
Lichtenauer M, Mildner M, Baumgartner A et al.: Intravenous and intramyocardial injection of apoptotic white blood cell suspensions prevents ventricular remodelling by increasing elastin expression in cardiac scar tissue after myocardial infarction. Basic Res Cardiol. Jun 106(4), 645–55 (2011)
Mizuno T, Mickle DA, Kiani CG et al. Overexpression of elastin fragments in infarcted myocardium attenuates scar expansion and heart dysfunction. Am J Physiol Heart Circ Physiol. 2005 Jun;288(6):H2819–27
Lichtenauer M, Mildner M, Hoetzenecker K et al. Secretome of apoptotic peripheral blood cells (APOSEC) confers cytoprotection to cardiomyocytes and inhibits tissue remodelling after acute myocardial infarction: a preclinical study. Basic Res Cardiol. 2011 [ahead of print]. doi:10.1007/s00395-011-0224-6
Korf-Klingebiel M, Kempf T, Sauer T et al.: Bone marrow cells are a rich source of growth factors and cytokines: implications for cell therapy trials after myocardial infarction. Eur Heart J. Dec 29(23), 2851–8 (2008)
Gnecchi M, Melo LG.: Bone marrow-derived mesenchymal stem cells: isolation, expansion, characterization, viral transduction, and production of conditioned medium. Methods Mol Biol. 482, 281–94 (2009)
Di Santo S, Yang Z, Wyler von Ballmoos M et al. Novel cell-free strategy for therapeutic angiogenesis: in vitro generated conditioned medium can replace progenitor cell transplantation. PLoS One. 2009 May 21;4(5):e5643
Timmers L, Lim SK, Hoefer IE et al.: Human mesenchymal stem cell-conditioned medium improves cardiac function following myocardial infarction. Stem Cell Res. May 6(3), 206–14 (2011)
Hausenloy DJ, Yellon DM.: Reperfusion injury salvage kinase signalling: taking a RISK for cardioprotection. Heart Fail Rev. Dec; 12(3–4), 217–34 (2007)
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Lichtenauer, M., Mildner, M., Gyöngyösi, M. et al. Apoptotische Leukozyten und deren Sekretionsprodukt. Wien klin Mag 14, 6–10 (2011). https://doi.org/10.1007/s00740-011-0403-y
Published:
Issue Date:
DOI: https://doi.org/10.1007/s00740-011-0403-y