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Pro-Angiogenic Macrophage Phenotype to Promote Myocardial Repair

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Pro-Angiogenic Macrophage Phenotype to Promote Myocardial Repair. / Ferraro, Bartolo; Leoni, Giovanna; Hinkel, Rabea; Ormanns, Steffen; Paulin, Nicole; Ortega-Gomez, Almudena; Viola, Joana R; de Jong, Renske; Bongiovanni, Dario; Bozoglu, Tarik; Maas, Sanne L; D'Amico, Michele; Kessler, Thorsten; Zeller, Tanja; Hristov, Michael; Reutelingsperger, Chris; Sager, Hendrik B; Döring, Yvonne; Nahrendorf, Matthias; Kupatt, Christian; Soehnlein, Oliver.

In: J AM COLL CARDIOL, Vol. 73, No. 23, 18.06.2019, p. 2990-3002.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Ferraro, B, Leoni, G, Hinkel, R, Ormanns, S, Paulin, N, Ortega-Gomez, A, Viola, JR, de Jong, R, Bongiovanni, D, Bozoglu, T, Maas, SL, D'Amico, M, Kessler, T, Zeller, T, Hristov, M, Reutelingsperger, C, Sager, HB, Döring, Y, Nahrendorf, M, Kupatt, C & Soehnlein, O 2019, 'Pro-Angiogenic Macrophage Phenotype to Promote Myocardial Repair', J AM COLL CARDIOL, vol. 73, no. 23, pp. 2990-3002. https://doi.org/10.1016/j.jacc.2019.03.503

APA

Ferraro, B., Leoni, G., Hinkel, R., Ormanns, S., Paulin, N., Ortega-Gomez, A., Viola, J. R., de Jong, R., Bongiovanni, D., Bozoglu, T., Maas, S. L., D'Amico, M., Kessler, T., Zeller, T., Hristov, M., Reutelingsperger, C., Sager, H. B., Döring, Y., Nahrendorf, M., ... Soehnlein, O. (2019). Pro-Angiogenic Macrophage Phenotype to Promote Myocardial Repair. J AM COLL CARDIOL, 73(23), 2990-3002. https://doi.org/10.1016/j.jacc.2019.03.503

Vancouver

Ferraro B, Leoni G, Hinkel R, Ormanns S, Paulin N, Ortega-Gomez A et al. Pro-Angiogenic Macrophage Phenotype to Promote Myocardial Repair. J AM COLL CARDIOL. 2019 Jun 18;73(23):2990-3002. https://doi.org/10.1016/j.jacc.2019.03.503

Bibtex

@article{a911d40f871a4871a6648b4e6cb19a89,
title = "Pro-Angiogenic Macrophage Phenotype to Promote Myocardial Repair",
abstract = "BACKGROUND: Heart failure following myocardial infarction (MI) remains one of the major causes of death worldwide, and its treatment is a crucial challenge of cardiovascular medicine. An attractive therapeutic strategy is to stimulate endogenous mechanisms of myocardial regeneration.OBJECTIVES: This study evaluates the potential therapeutic treatment with annexin A1 (AnxA1) to induce cardiac repair after MI.METHODS: AnxA1 knockout (AnxA1-/-) and wild-type mice underwent MI induced by ligation of the left anterior descending coronary artery. Cardiac functionality was assessed by longitudinal echocardiographic measurements. Histological, fluorescence-activated cell sorting, dot blot analysis, and in vitro/ex vivo studies were used to assess the myocardial neovascularization, macrophage content, and activity in response to AnxA1.RESULTS: AnxA1-/- mice showed a reduced cardiac functionality and an expansion of proinflammatory macrophages in the ischemic area. Cardiac macrophages from AnxA1-/- mice exhibited a dramatically reduced ability to release the proangiogenic mediator vascular endothelial growth factor (VEGF)-A. However, AnxA1 treatment enhanced VEGF-A release from cardiac macrophages, and its delivery in vivo markedly improved cardiac performance. The positive effect of AnxA1 treatment on cardiac performance was abolished in wild-type mice transplanted with bone marrow derived from Cx3cr1creERT2Vegfflox/flox or in mice depleted of macrophages. Similarly, cardioprotective effects of AnxA1 were obtained in pigs in which full-length AnxA1 was overexpressed by use of a cardiotropic adeno-associated virus.CONCLUSIONS: AnxA1 has a direct action on cardiac macrophage polarization toward a pro-angiogenic, reparative phenotype. AnxA1 stimulated cardiac macrophages to release high amounts of VEGF-A, thus inducing neovascularization and cardiac repair.",
keywords = "Animals, Annexin A1/deficiency, Female, Macrophages/physiology, Mice, Mice, Inbred C57BL, Mice, Knockout, Myocardial Infarction/genetics, Myocardium/metabolism, Neovascularization, Physiologic/physiology, Phenotype",
author = "Bartolo Ferraro and Giovanna Leoni and Rabea Hinkel and Steffen Ormanns and Nicole Paulin and Almudena Ortega-Gomez and Viola, {Joana R} and {de Jong}, Renske and Dario Bongiovanni and Tarik Bozoglu and Maas, {Sanne L} and Michele D'Amico and Thorsten Kessler and Tanja Zeller and Michael Hristov and Chris Reutelingsperger and Sager, {Hendrik B} and Yvonne D{\"o}ring and Matthias Nahrendorf and Christian Kupatt and Oliver Soehnlein",
note = "Copyright {\textcopyright} 2019 The Authors. Published by Elsevier Inc. All rights reserved.",
year = "2019",
month = jun,
day = "18",
doi = "10.1016/j.jacc.2019.03.503",
language = "English",
volume = "73",
pages = "2990--3002",
journal = "J AM COLL CARDIOL",
issn = "0735-1097",
publisher = "Elsevier USA",
number = "23",

}

RIS

TY - JOUR

T1 - Pro-Angiogenic Macrophage Phenotype to Promote Myocardial Repair

AU - Ferraro, Bartolo

AU - Leoni, Giovanna

AU - Hinkel, Rabea

AU - Ormanns, Steffen

AU - Paulin, Nicole

AU - Ortega-Gomez, Almudena

AU - Viola, Joana R

AU - de Jong, Renske

AU - Bongiovanni, Dario

AU - Bozoglu, Tarik

AU - Maas, Sanne L

AU - D'Amico, Michele

AU - Kessler, Thorsten

AU - Zeller, Tanja

AU - Hristov, Michael

AU - Reutelingsperger, Chris

AU - Sager, Hendrik B

AU - Döring, Yvonne

AU - Nahrendorf, Matthias

AU - Kupatt, Christian

AU - Soehnlein, Oliver

N1 - Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2019/6/18

Y1 - 2019/6/18

N2 - BACKGROUND: Heart failure following myocardial infarction (MI) remains one of the major causes of death worldwide, and its treatment is a crucial challenge of cardiovascular medicine. An attractive therapeutic strategy is to stimulate endogenous mechanisms of myocardial regeneration.OBJECTIVES: This study evaluates the potential therapeutic treatment with annexin A1 (AnxA1) to induce cardiac repair after MI.METHODS: AnxA1 knockout (AnxA1-/-) and wild-type mice underwent MI induced by ligation of the left anterior descending coronary artery. Cardiac functionality was assessed by longitudinal echocardiographic measurements. Histological, fluorescence-activated cell sorting, dot blot analysis, and in vitro/ex vivo studies were used to assess the myocardial neovascularization, macrophage content, and activity in response to AnxA1.RESULTS: AnxA1-/- mice showed a reduced cardiac functionality and an expansion of proinflammatory macrophages in the ischemic area. Cardiac macrophages from AnxA1-/- mice exhibited a dramatically reduced ability to release the proangiogenic mediator vascular endothelial growth factor (VEGF)-A. However, AnxA1 treatment enhanced VEGF-A release from cardiac macrophages, and its delivery in vivo markedly improved cardiac performance. The positive effect of AnxA1 treatment on cardiac performance was abolished in wild-type mice transplanted with bone marrow derived from Cx3cr1creERT2Vegfflox/flox or in mice depleted of macrophages. Similarly, cardioprotective effects of AnxA1 were obtained in pigs in which full-length AnxA1 was overexpressed by use of a cardiotropic adeno-associated virus.CONCLUSIONS: AnxA1 has a direct action on cardiac macrophage polarization toward a pro-angiogenic, reparative phenotype. AnxA1 stimulated cardiac macrophages to release high amounts of VEGF-A, thus inducing neovascularization and cardiac repair.

AB - BACKGROUND: Heart failure following myocardial infarction (MI) remains one of the major causes of death worldwide, and its treatment is a crucial challenge of cardiovascular medicine. An attractive therapeutic strategy is to stimulate endogenous mechanisms of myocardial regeneration.OBJECTIVES: This study evaluates the potential therapeutic treatment with annexin A1 (AnxA1) to induce cardiac repair after MI.METHODS: AnxA1 knockout (AnxA1-/-) and wild-type mice underwent MI induced by ligation of the left anterior descending coronary artery. Cardiac functionality was assessed by longitudinal echocardiographic measurements. Histological, fluorescence-activated cell sorting, dot blot analysis, and in vitro/ex vivo studies were used to assess the myocardial neovascularization, macrophage content, and activity in response to AnxA1.RESULTS: AnxA1-/- mice showed a reduced cardiac functionality and an expansion of proinflammatory macrophages in the ischemic area. Cardiac macrophages from AnxA1-/- mice exhibited a dramatically reduced ability to release the proangiogenic mediator vascular endothelial growth factor (VEGF)-A. However, AnxA1 treatment enhanced VEGF-A release from cardiac macrophages, and its delivery in vivo markedly improved cardiac performance. The positive effect of AnxA1 treatment on cardiac performance was abolished in wild-type mice transplanted with bone marrow derived from Cx3cr1creERT2Vegfflox/flox or in mice depleted of macrophages. Similarly, cardioprotective effects of AnxA1 were obtained in pigs in which full-length AnxA1 was overexpressed by use of a cardiotropic adeno-associated virus.CONCLUSIONS: AnxA1 has a direct action on cardiac macrophage polarization toward a pro-angiogenic, reparative phenotype. AnxA1 stimulated cardiac macrophages to release high amounts of VEGF-A, thus inducing neovascularization and cardiac repair.

KW - Animals

KW - Annexin A1/deficiency

KW - Female

KW - Macrophages/physiology

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Myocardial Infarction/genetics

KW - Myocardium/metabolism

KW - Neovascularization, Physiologic/physiology

KW - Phenotype

U2 - 10.1016/j.jacc.2019.03.503

DO - 10.1016/j.jacc.2019.03.503

M3 - SCORING: Journal article

C2 - 31196457

VL - 73

SP - 2990

EP - 3002

JO - J AM COLL CARDIOL

JF - J AM COLL CARDIOL

SN - 0735-1097

IS - 23

ER -