CCR6 Deficiency Increases Infarct Size after Murine Acute Myocardial Infarction.
CCR6 Deficiency Increases Infarct Size after Murine Acute Myocardial Infarction.
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DOI：
10.3390/biomedicines9111532
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发表时间：
2021-10-25
期刊：
影响因子：
4.7
通讯作者：
van der Vorst EPC
中科院分区：
文献类型：
--
作者：
Schumacher D;Liehn EA;Singh A;Curaj A;Wijnands E;Lira SA;Tacke F;Jankowski J;Biessen EAL;van der Vorst EPC
闭塞的冠状动脉再开放后的缺血再灌注损伤是急性心肌梗死后心脏损伤和炎症的主要原因。趋化因子轴CCL 20-CCR 6是各种炎症过程中的关键参与者，包括动脉粥样硬化;然而，其在缺血-再灌注损伤中的作用仍然难以捉摸。因此，为了更深入地了解CCR 6在急性心肌梗死中的作用，我们研究了Ccr 6 −/−小鼠及其相应的C57 Bl/6野生型对照动物短暂结扎冠状动脉左前降支后再灌注的心脏损伤。令人惊讶的是，Ccr 6 −/−小鼠在缺血/再灌注后表现出显著降低的心脏功能和增加的梗死面积。这与心脏炎症的显著增加相一致，其特征在于中性粒细胞和炎性巨噬细胞积聚。骨髓缺乏CCR 6的嵌合体反映了这种不利的Ccr 6 −/−表型，而心脏损伤在基质CCR 6缺乏的嵌合体中没有变化。这项研究表明，CCR 6依赖性（骨髓）细胞在心肌梗死和随后的缺血再灌注损伤中发挥保护作用，支持增强CCR 6依赖性免疫机制是一个有趣的治疗靶点的观点。
Ischemia-reperfusion injury after the reopening of an occluded coronary artery is a major cause of cardiac damage and inflammation after acute myocardial infarction. The chemokine axis CCL20-CCR6 is a key player in various inflammatory processes, including atherosclerosis; however, its role in ischemia-reperfusion injury has remained elusive. Therefore, to gain more insight into the role of the CCR6 in acute myocardial infarction, we have studied cardiac injury after transient ligation of the left anterior descending coronary artery followed by reperfusion in Ccr6−/− mice and their respective C57Bl/6 wild-type controls. Surprisingly, Ccr6−/− mice demonstrated significantly reduced cardiac function and increased infarct sizes after ischemia/reperfusion. This coincided with a significant increase in cardiac inflammation, characterized by an accumulation of neutrophils and inflammatory macrophage accumulation. Chimeras with a bone marrow deficiency of CCR6 mirrored this adverse Ccr6−/− phenotype, while cardiac injury was unchanged in chimeras with stromal CCR6 deficiency. This study demonstrates that CCR6-dependent (bone marrow) cells exert a protective role in myocardial infarction and subsequent ischemia-reperfusion injury, supporting the notion that augmenting CCR6-dependent immune mechanisms represents an interesting therapeutic target.
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影响因子：
2.5
作者：
Li R;Frangogiannis NG
通讯作者：
Frangogiannis NG
DOI：
10.2353/ajpath.2010.090759
发表时间：
2010-05
期刊：
The American journal of pathology
影响因子：
--
作者：
Dobaczewski M;Xia Y;Bujak M;Gonzalez-Quesada C;Frangogiannis NG
通讯作者：
Frangogiannis NG
DOI：
10.15190/d.2016.13
发表时间：
2016-09-30
期刊：
Discoveries (Craiova, Romania)
影响因子：
--
作者：
Curaj, Adelina;Pop-Fele, Lucian;Liehn, Elisa A
通讯作者：
Liehn, Elisa A
影响因子：
4
作者：
Reimer, Dorothea;Lee, Adrian Y. S.;Koerner, Heinrich
通讯作者：
Koerner, Heinrich
内皮 CXCR7 的缺失会损害心肌梗死后的血管稳态和心脏重塑对心血管药物发现的影响
影响因子：
37.8
作者：
Hao, Huifeng;Hu, Sheng;Wang, Miao
通讯作者：
Wang, Miao