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CCR3 and myocardial infarction

DISCOVERIES (ISSN 2359-7232), 2015, April-June issue

CITATION: 

Curaj A, Staudt M, Fatu R, Kraaijeveld AO, Jankowski J, Biessen EAL, Liehn EA. Blockade of CCR3 retains the neutrophils, preserving their survival during healing after myocardial infarction. Discoveries 2015, 3: e45. DOI: 10.15190/d.2015.37

 Submitted: June 20, 2015; Revised: June 29; Accepted: June 30, 2015Published: June 30, 2015;

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Blockade of CCR3 retains the neutrophils, preserving their survival during healing after myocardial infarction

Adelina Curaj (1,2), Mareike Staudt (1), Roxana Fatu (1), Andreas O. Kraaijeveld (3), Joachim Jankowski (1), Erik A.L. Biessen (4), Elisa A. Liehn (1,*)

(1) Institute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, Germany
(2) Victor Babes National Institute of Pathology, Bucharest, Romania
(3) Department of Cardiology and Einthoven Laboratory of Experimental Vascular Medicine, Leiden University Medical Center, The Netherlands;
(4) Department of Pathology, Academic University Hospital Maastricht, Maastricht, The Netherlands

*Correspondence to: Elisa A. Liehn, MD, PhD, Institute for Molecular Cardiovascular Research, University Hospital Aachen, Germany; Phone: +49-241-80 35983; Fax: +49-241-80 82716; Email: eliehn@ukaachen.de

Abstract

BACKGROUND: Chemokines are critical mediators in controlling and monitoring the healing and ventricular remodeling after myocardial infarction (MI). They proved to be valuable pharmacological targets for novel therapeutic strategies to reduce the scar formation and to sustain the heart function in patients suffering MI. In the present study, we aim to establish the role of CCR3 in myocardial ischemia/reperfusion.
METHODS AND RESULTS: One week after ischemia/reperfusion induction in a mouse model, the functional and morphological parameters of the heart were analyzed. Isolated-heart perfusion (Langendorff model) showed no significant differences in heart function, infarction size and angiogenesis after pharmacological blockade of CCR3. Notably, a massive neutrophil infiltration was detected in the anti-CCR3 treated group compared to control group. Other immune cells subsets, as well as apoptotic or proliferation signals and collagen synthesis were not affected.
CONCLUSION: Since targeting neutrophils represents one of the most studied therapeutic strategy, this study opens a new perspective for better understanding the physiology and homeostasis of neutrophils, and points out a new research direction which may be of benefit for the patients with myocardial infarction

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