Web of Science: 32 cites, Scopus: 34 cites, Google Scholar: cites,
Bone marrow endothelial dysfunction promotes myeloid cell expansion in cardiovascular disease
Rohde, David (Harvard Medical School)
Vandoorne, Katrien (Harvard Medical School)
Lee, I-Hsiu (Massachusetts General Hospital (Boston))
Grune, Jana (Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA)
Zhang, Shuang (Massachusetts General Hospital (Boston))
McAlpine, Cameron S. (Massachusetts General Hospital (Boston))
Schloss, Maximilian J. (Massachusetts General Hospital (Boston))
Nayar, Ribhu (Massachusetts General Hospital (Boston))
Courties, Gabriel (Massachusetts General Hospital (Boston))
Frodermann, Vanessa (Massachusetts General Hospital (Boston))
Wojtkiewicz, Gregory (Massachusetts General Hospital (Boston))
Honold, Lisa (Massachusetts General Hospital (Boston))
Chen, Qi (Max Planck Institute for Molecular Biomedicine, Muenster, Germany)
Schmidt, Stephen (Massachusetts General Hospital (Boston))
Iwamoto, Yoshiko (Massachusetts General Hospital (Boston))
Sun, Yuan (Massachusetts General Hospital (Boston))
Cremer, Sebastian (Massachusetts General Hospital (Boston))
Hoyer, Friedrich F. (Massachusetts General Hospital (Boston))
Iborra Egea, Oriol (Institut Germans Trias i Pujol)
Muñoz-Guijosa, Christian (Institut Germans Trias i Pujol)
Ji, Fei (Department of Molecular Biology, Massachusetts General Hospital)
Zhou, Bin (Chinese Academy of Sciences)
Adams, Ralf H. (Max Planck Institute for Molecular Biomedicine (Alemanya))
Wythe, Joshua D. (Department of Molecular Physiology and Biophysics, Baylor College of Medicine (Estats Units d'Amèrica))
Hidalgo Pareja, Juan (Universitat Autònoma de Barcelona. Institut de Neurociències)
Watanabe, Hideto (Aichi Medical University)
Jung, Yookyung (Massachusetts General Hospital (Boston))
van der Laan, Anja M. (Department of Cardiology, University of Amsterdam)
Piek, Jan J. (Department of Cardiology, University of Amsterdam)
Kfoury, Youmna (Department of Stem Cell and Regenerative Biology, Harvard University)
Désogère, Pauline A. (Harvard Medical School)
Vinegoni, Claudio (Massachusetts General Hospital (Boston))
Dutta, Partha (Department of Medicine, University of Pittsburgh School of Medicine)
Sadreyev, Ruslan I. (Harvard Medical School)
Caravan, Peter (Harvard Medical School)
Bayés-Genís, Antoni (Institut Germans Trias i Pujol)
Libby, Peter (righam and Women's Hospital (Boston, Estats Units d'Amèrica))
Scadden, David T. (Department of Stem Cell and Regenerative Biology, Harvard University)
Lin, Charles P. (Aichi Medical University)
Naxerova, Kamila (Massachusetts General Hospital (Boston))
Swirski, Filip K. (Massachusetts General Hospital (Boston))
Nahrendorf, Matthias (Department of Internal Medicine I, University Hospital Wuerzburg)

Data: 2021
Resum: Abnormal hematopoiesis advances cardiovascular disease by generating excess inflammatory leukocytes that attack the arteries and the heart. The bone marrow niche regulates hematopoietic stem cell proliferation and hence the systemic leukocyte pool, but whether cardiovascular disease affects the hematopoietic organ's microvasculature is unknown. Here we show that hypertension, atherosclerosis and myocardial infarction (MI) instigate endothelial dysfunction, leakage, vascular fibrosis and angiogenesis in the bone marrow, altogether leading to overproduction of inflammatory myeloid cells and systemic leukocytosis. Limiting angiogenesis with endothelial deletion of Vegfr2 (encoding vascular endothelial growth factor (VEGF) receptor 2) curbed emergency hematopoiesis after MI. We noted that bone marrow endothelial cells assumed inflammatory transcriptional phenotypes in all examined stages of cardiovascular disease. Endothelial deletion of Il6 or Vcan (encoding versican), genes shown to be highly expressed in mice with atherosclerosis or MI, reduced hematopoiesis and systemic myeloid cell numbers in these conditions. Our findings establish that cardiovascular disease remodels the vascular bone marrow niche, stimulating hematopoiesis and production of inflammatory leukocytes.
Ajuts: Ministerio de Economía y Competitividad SAF2014-56546-R
Agencia Estatal de Investigación RTI2018-101105-B-I00
Drets: Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original. Creative Commons
Llengua: Anglès
Document: Article ; recerca ; Versió publicada
Publicat a: Nature cardiovascular research, Vol. 1 (december 2021) , p. 28-44, ISSN 2731-0590

DOI: 10.1038/s44161-021-00002-8
PMID: 35747128


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Documents de recerca > Documents dels grups de recerca de la UAB > Centres i grups de recerca (producció científica) > Ciències de la salut i biociències > Institut d'Investigació en Ciencies de la Salut Germans Trias i Pujol (IGTP)
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 Registre creat el 2023-09-27, darrera modificació el 2024-06-11



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