血管生成
生物
酪氨酸激酶
受体酪氨酸激酶
癌症研究
内皮干细胞
细胞生物学
受体
内科学
信号转导
免疫学
医学
生物化学
体外
作者
Marc R. Reboll,Stefanie Klede,Manuel H. Taft,Chen-Leng Cai,Loren J. Field,Kory J. Lavine,Andrew L. Koenig,Jenni Fleischauer,Johann Meyer,Axel Schambach,Hans W.M. Niessen,Maike Kosanke,Joop van den Heuvel,Andreas Pich,Johann Bauersachs,Xuekun Wu,Linqun Zheng,Yong Wang,Mortimer Korf‐Klingebiel,Felix Polten,Kai C. Wollert
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2022-06-17
卷期号:376 (6599): 1343-1347
被引量:35
标识
DOI:10.1126/science.abn3027
摘要
Effective tissue repair after myocardial infarction entails a vigorous angiogenic response, guided by incompletely defined immune cell–endothelial cell interactions. We identify the monocyte- and macrophage-derived cytokine METRNL (meteorin-like) as a driver of postinfarction angiogenesis and high-affinity ligand for the stem cell factor receptor KIT (KIT receptor tyrosine kinase). METRNL mediated angiogenic effects in cultured human endothelial cells through KIT-dependent signaling pathways. In a mouse model of myocardial infarction, METRNL promoted infarct repair by selectively expanding the KIT-expressing endothelial cell population in the infarct border zone. Metrnl -deficient mice failed to mount this KIT-dependent angiogenic response and developed severe postinfarction heart failure. Our data establish METRNL as a KIT receptor ligand in the context of ischemic tissue repair.
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