Why the study?
Does CCR3 blockade improve functional and morphological parameters in a mouse model of myocardial infarction?
Does CCR3 blockade improve functional and morphological parameters in a mouse model of myocardial infarction?
CCR3 blockade in a mouse model of myocardial infarction does not affect infarct size or cardiac function but causes massive neutrophil infiltration, highlighting its role in neutrophil homeostasis.
CCR3 blockade yields no post-MI benefit in mice; leaves open its role in neutrophil homeostasis.
BACKGROUND: Chemokines are critical mediators in controlling and monitoring the healing and ventricular remodeling after myocardial infarction (MI). They proved to be valuable targets for therapeutic measures to reduce the scar formation and to preserve heart function in patients suffering MI. In the present study, the role of CCR3 in myocardial ischemia/reperfusion was established. METHODS AND RESULTS: One week after infarct induction in a mouse coronary ligation model, the functional and morphological parameters of the heart were analyzed. Isolated-heart Langendorff perfusion showed no significantly differences in heart function, infarction size and post infarction angiogenesis after CCR3 blockade. Apoptotic, proliferation signals as well as collagen synthesis were not affected in CCR3 antagonist treated mice. Notably, CCR3 inhibition was accompanied by massive neutrophil infiltration, while leaving the presence of other immune cell subsets in heart unaffected. CONCLUSION: Since neutrophils represents one of the most widely explored therapeutic targets in the treatment of cardiac disease, this study may open a new perspective for a better understanding of the physiology and homeostasis of neutrophils and points out new directions for intervention in acute MI.
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Curaj et al. (2015) studied this question.
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