Anti-thymocyte globulin induces neoangiogenesis and preserves cardiac function after experimental myocardial infarction.

<h4>Rationale</h4>Acute myocardial infarction (AMI) followed by ventricular remodeling is the major cause of congestive heart failure and death in western world countries.<h4>Objective</h4>Of relevance are reports showing that infusion of apoptotic leucocytes or anti-lymphocy...

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Autores principales:	Michael Lichtenauer, Michael Mildner, Gregor Werba, Lucian Beer, Konrad Hoetzenecker, Andrea Baumgartner, Matthias Hasun, Stefanie Nickl, Andreas Mitterbauer, Matthias Zimmermann, Mariann Gyöngyösi, Bruno Karl Podesser, Walter Klepetko, Hendrik Jan Ankersmit
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/54c1018b841440db976663e6af0e0bac
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spelling	oai:doaj.org-article:54c1018b841440db976663e6af0e0bac2021-11-18T08:04:19ZAnti-thymocyte globulin induces neoangiogenesis and preserves cardiac function after experimental myocardial infarction.1932-620310.1371/journal.pone.0052101https://doaj.org/article/54c1018b841440db976663e6af0e0bac2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23284885/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Rationale</h4>Acute myocardial infarction (AMI) followed by ventricular remodeling is the major cause of congestive heart failure and death in western world countries.<h4>Objective</h4>Of relevance are reports showing that infusion of apoptotic leucocytes or anti-lymphocyte serum after AMI reduces myocardial necrosis and preserves cardiac function. In order to corroborate this therapeutic mechanism, the utilization of an immunosuppressive agent with a comparable mechanism, such as anti-thymocyte globulin (ATG) was evaluated in this study.<h4>Methods and results</h4>AMI was induced in rats by ligation of the left anterior descending artery. Initially after the onset of ischemia, rabbit ATG (10 mg/rat) was injected intravenously. In vitro and in vivo experiments showed that ATG induced a pronounced release of pro-angiogenic and chemotactic factors. Moreover, paracrine factors released from ATG co-incubated cell cultures conferred a down-regulation of p53 in cardiac myocytes. Rats that were injected with ATG evidenced higher numbers of CD68+ macrophages in the ischemic myocardium. Animals injected with ATG evidenced less myocardial necrosis, showed a significant reduction of infarct dimension and an improvement of post-AMI remodeling after six weeks (infarct dimension 24.9% vs. 11.4%, p<0.01). Moreover, a higher vessel density in the peri-infarct region indicated a better collateralization in rats that were injected with ATG.<h4>Conclusions</h4>These data indicate that ATG, a therapeutic agent successfully applied in clinical transplant immunology, triggered cardioprotective effects after AMI that salvaged ischemic myocardium by down-regulation of p53. This might have raised the resistance against apoptotic cell death during ischemia. The combination of these mechanisms seems to be causative for improved cardiac function and less ventricular remodeling after experimental AMI.Michael LichtenauerMichael LichtenauerMichael MildnerGregor WerbaLucian BeerKonrad HoetzeneckerAndrea BaumgartnerMatthias HasunStefanie NicklAndreas MitterbauerMatthias ZimmermannMariann GyöngyösiBruno Karl PodesserWalter KlepetkoHendrik Jan AnkersmitPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 12, p e52101 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Michael Lichtenauer Michael Lichtenauer Michael Mildner Gregor Werba Lucian Beer Konrad Hoetzenecker Andrea Baumgartner Matthias Hasun Stefanie Nickl Andreas Mitterbauer Matthias Zimmermann Mariann Gyöngyösi Bruno Karl Podesser Walter Klepetko Hendrik Jan Ankersmit Anti-thymocyte globulin induces neoangiogenesis and preserves cardiac function after experimental myocardial infarction.
description	<h4>Rationale</h4>Acute myocardial infarction (AMI) followed by ventricular remodeling is the major cause of congestive heart failure and death in western world countries.<h4>Objective</h4>Of relevance are reports showing that infusion of apoptotic leucocytes or anti-lymphocyte serum after AMI reduces myocardial necrosis and preserves cardiac function. In order to corroborate this therapeutic mechanism, the utilization of an immunosuppressive agent with a comparable mechanism, such as anti-thymocyte globulin (ATG) was evaluated in this study.<h4>Methods and results</h4>AMI was induced in rats by ligation of the left anterior descending artery. Initially after the onset of ischemia, rabbit ATG (10 mg/rat) was injected intravenously. In vitro and in vivo experiments showed that ATG induced a pronounced release of pro-angiogenic and chemotactic factors. Moreover, paracrine factors released from ATG co-incubated cell cultures conferred a down-regulation of p53 in cardiac myocytes. Rats that were injected with ATG evidenced higher numbers of CD68+ macrophages in the ischemic myocardium. Animals injected with ATG evidenced less myocardial necrosis, showed a significant reduction of infarct dimension and an improvement of post-AMI remodeling after six weeks (infarct dimension 24.9% vs. 11.4%, p<0.01). Moreover, a higher vessel density in the peri-infarct region indicated a better collateralization in rats that were injected with ATG.<h4>Conclusions</h4>These data indicate that ATG, a therapeutic agent successfully applied in clinical transplant immunology, triggered cardioprotective effects after AMI that salvaged ischemic myocardium by down-regulation of p53. This might have raised the resistance against apoptotic cell death during ischemia. The combination of these mechanisms seems to be causative for improved cardiac function and less ventricular remodeling after experimental AMI.
format	article
author	Michael Lichtenauer Michael Lichtenauer Michael Mildner Gregor Werba Lucian Beer Konrad Hoetzenecker Andrea Baumgartner Matthias Hasun Stefanie Nickl Andreas Mitterbauer Matthias Zimmermann Mariann Gyöngyösi Bruno Karl Podesser Walter Klepetko Hendrik Jan Ankersmit
author_facet	Michael Lichtenauer Michael Lichtenauer Michael Mildner Gregor Werba Lucian Beer Konrad Hoetzenecker Andrea Baumgartner Matthias Hasun Stefanie Nickl Andreas Mitterbauer Matthias Zimmermann Mariann Gyöngyösi Bruno Karl Podesser Walter Klepetko Hendrik Jan Ankersmit
author_sort	Michael Lichtenauer
title	Anti-thymocyte globulin induces neoangiogenesis and preserves cardiac function after experimental myocardial infarction.
title_short	Anti-thymocyte globulin induces neoangiogenesis and preserves cardiac function after experimental myocardial infarction.
title_full	Anti-thymocyte globulin induces neoangiogenesis and preserves cardiac function after experimental myocardial infarction.
title_fullStr	Anti-thymocyte globulin induces neoangiogenesis and preserves cardiac function after experimental myocardial infarction.
title_full_unstemmed	Anti-thymocyte globulin induces neoangiogenesis and preserves cardiac function after experimental myocardial infarction.
title_sort	anti-thymocyte globulin induces neoangiogenesis and preserves cardiac function after experimental myocardial infarction.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/54c1018b841440db976663e6af0e0bac
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Anti-thymocyte globulin induces neoangiogenesis and preserves cardiac function after experimental myocardial infarction.

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