Curaj Adelina, Staudt Mareike, Fatu Roxana, Kraaijeveld Andreas O, Jankowski Joachim, Biessen Erik A L, Liehn Elisa A
Institute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, Germany.
"Victor Babes" National Institute of Pathology, Bucharest, Romania.
Discoveries (Craiova). 2015 Jun 30;3(2):e45. doi: 10.15190/d.2015.37.
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.
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.
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.
趋化因子是控制和监测心肌梗死（MI）后愈合及心室重塑的关键介质。它们已被证明是减少瘢痕形成和保护MI患者心脏功能的治疗措施的重要靶点。在本研究中，确定了CCR3在心肌缺血/再灌注中的作用。
在小鼠冠状动脉结扎模型中诱导梗死一周后，分析心脏的功能和形态学参数。离体心脏Langendorff灌注显示，CCR3阻断后心脏功能、梗死面积和梗死后血管生成无显著差异。CCR3拮抗剂处理的小鼠中，凋亡、增殖信号以及胶原蛋白合成均未受影响。值得注意的是，CCR3抑制伴随着大量中性粒细胞浸润，而心脏中其他免疫细胞亚群的存在未受影响。
由于中性粒细胞是心脏病治疗中研究最广泛的治疗靶点之一，本研究可能为更好地理解中性粒细胞的生理学和内环境稳定开辟新的视角，并为急性心肌梗死的干预指出新的方向。
