Meteorin-like promotes heart repair through endothelial KIT receptor tyrosine kinase.

Autor: Reboll MR; Division of Molecular and Translational Cardiology, Hans Borst Center for Heart and Stem Cell Research, Hannover Medical School, 30625 Hannover, Germany.; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany., Klede S; Division of Molecular and Translational Cardiology, Hans Borst Center for Heart and Stem Cell Research, Hannover Medical School, 30625 Hannover, Germany.; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany., Taft MH; Institute for Biophysical Chemistry, Hannover Medical School, 30625 Hannover, Germany., Cai CL; Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA., Field LJ; Krannert Cardiovascular Research Center and the Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA., Lavine KJ; Center for Cardiovascular Research, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA., Koenig AL; Center for Cardiovascular Research, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA., Fleischauer J; Institute of Experimental Hematology, Hannover Medical School, 30625 Hannover, Germany., Meyer J; Institute of Experimental Hematology, Hannover Medical School, 30625 Hannover, Germany., Schambach A; Institute of Experimental Hematology, Hannover Medical School, 30625 Hannover, Germany., Niessen HW; Department of Pathology and Department of Cardiac Surgery, Institute for Cardiovascular Research, Amsterdam University Medical Center, 1007 MB Amsterdam, Netherlands., Kosanke M; Research Core Unit Genomics, Hannover Medical School, 30625 Hannover, Germany., van den Heuvel J; Technology Platform Recombinant Protein Expression, Helmholtz Center for Infection Research, 38124 Braunschweig, Germany., Pich A; Core Unit Proteomics and Institute of Toxicology, Hannover Medical School, 30625 Hannover, Germany., Bauersachs J; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany., Wu X; Division of Molecular and Translational Cardiology, Hans Borst Center for Heart and Stem Cell Research, Hannover Medical School, 30625 Hannover, Germany.; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany., Zheng L; Division of Molecular and Translational Cardiology, Hans Borst Center for Heart and Stem Cell Research, Hannover Medical School, 30625 Hannover, Germany.; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany., Wang Y; Division of Molecular and Translational Cardiology, Hans Borst Center for Heart and Stem Cell Research, Hannover Medical School, 30625 Hannover, Germany.; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany., Korf-Klingebiel M; Division of Molecular and Translational Cardiology, Hans Borst Center for Heart and Stem Cell Research, Hannover Medical School, 30625 Hannover, Germany.; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany., Polten F; Division of Molecular and Translational Cardiology, Hans Borst Center for Heart and Stem Cell Research, Hannover Medical School, 30625 Hannover, Germany.; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany., Wollert KC; Division of Molecular and Translational Cardiology, Hans Borst Center for Heart and Stem Cell Research, Hannover Medical School, 30625 Hannover, Germany.; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany.
Jazyk: angličtina
Zdroj: Science (New York, N.Y.) [Science] 2022 Jun 17; Vol. 376 (6599), pp. 1343-1347. Date of Electronic Publication: 2022 Jun 16.
DOI: 10.1126/science.abn3027
Abstrakt: 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.
Databáze: MEDLINE
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