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Exercise reduces inflammatory cell production and cardiovascular inflammation via instruction of hematopoietic progenitor cells.
Frodermann, Vanessa; Rohde, David; Courties, Gabriel; Severe, Nicolas; Schloss, Maximilian J; Amatullah, Hajera; McAlpine, Cameron S; Cremer, Sebastian; Hoyer, Friedrich F; Ji, Fei; van Koeverden, Ian D; Herisson, Fanny; Honold, Lisa; Masson, Gustavo Santos; Zhang, Shuang; Grune, Jana; Iwamoto, Yoshiko; Schmidt, Stephen P; Wojtkiewicz, Gregory R; Lee, I-Hsiu; Gustafsson, Karin; Pasterkamp, Gerard; de Jager, Saskia C A; Sadreyev, Ruslan I; MacFadyen, Jean; Libby, Peter; Ridker, Paul; Scadden, David T; Naxerova, Kamila; Jeffrey, Kate L; Swirski, Filip K; Nahrendorf, Matthias.
Afiliação
  • Frodermann V; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Rohde D; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Courties G; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Severe N; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.
  • Schloss MJ; Center for Regenerative Medicine and Cancer Center, Massachusetts General Hospital, Boston, MA, USA.
  • Amatullah H; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • McAlpine CS; Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Cremer S; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Hoyer FF; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Ji F; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • van Koeverden ID; Department of Genetics, Harvard Medical School, Boston, MA, USA.
  • Herisson F; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA.
  • Honold L; Laboratory of Experimental Cardiology, Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands.
  • Masson GS; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Zhang S; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Grune J; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Iwamoto Y; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Schmidt SP; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Wojtkiewicz GR; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Lee IH; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Gustafsson K; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Pasterkamp G; Center for Systems Biology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • de Jager SCA; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.
  • Sadreyev RI; Center for Regenerative Medicine and Cancer Center, Massachusetts General Hospital, Boston, MA, USA.
  • MacFadyen J; Laboratory for Clinical Chemistry and Haematology, University Medical Center Utrecht, Utrecht, the Netherlands.
  • Libby P; Laboratory of Experimental Cardiology, Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands.
  • Ridker P; Laboratory of Translational Immunology, University Medical Center Utrecht, Utrecht, the Netherlands.
  • Scadden DT; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA.
  • Naxerova K; Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Jeffrey KL; Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
  • Swirski FK; Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
  • Nahrendorf M; Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Nat Med ; 25(11): 1761-1771, 2019 11.
Article em En | MEDLINE | ID: mdl-31700184
ABSTRACT
A sedentary lifestyle, chronic inflammation and leukocytosis increase atherosclerosis; however, it remains unclear whether regular physical activity influences leukocyte production. Here we show that voluntary running decreases hematopoietic activity in mice. Exercise protects mice and humans with atherosclerosis from chronic leukocytosis but does not compromise emergency hematopoiesis in mice. Mechanistically, exercise diminishes leptin production in adipose tissue, augmenting quiescence-promoting hematopoietic niche factors in leptin-receptor-positive stromal bone marrow cells. Induced deletion of the leptin receptor in Prrx1-creERT2; Leprfl/fl mice reveals that leptin's effect on bone marrow niche cells regulates hematopoietic stem and progenitor cell (HSPC) proliferation and leukocyte production, as well as cardiovascular inflammation and outcomes. Whereas running wheel withdrawal quickly reverses leptin levels, the impact of exercise on leukocyte production and on the HSPC epigenome and transcriptome persists for several weeks. Together, these data show that physical activity alters HSPCs via modulation of their niche, reducing hematopoietic output of inflammatory leukocytes.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Condicionamento Físico Animal / Células-Tronco Hematopoéticas / Doenças Cardiovasculares / Aterosclerose / Inflamação Limite: Animals / Humans Idioma: En Revista: Nat Med Assunto da revista: BIOLOGIA MOLECULAR / MEDICINA Ano de publicação: 2019 Tipo de documento: Article País de afiliação: Estados Unidos
Texto completo
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Condicionamento Físico Animal / Células-Tronco Hematopoéticas / Doenças Cardiovasculares / Aterosclerose / Inflamação Limite: Animals / Humans Idioma: En Revista: Nat Med Assunto da revista: BIOLOGIA MOLECULAR / MEDICINA Ano de publicação: 2019 Tipo de documento: Article País de afiliação: Estados Unidos