Myocardial infarction accelerates atherosclerosis

Partha Dutta, Gabriel Courties, Ying Wei, Florian Leuschner, Rostic Gorbatov, Clinton S. Robbins, Yoshiko Iwamoto, Brian Thompson, Alicia L. Carlson, Timo Heidt, Maulik D. Majmudar, Felix Lasitschka, Martin Etzrodt, Peter Waterman, Michael T. Waring, Adam T. Chicoine, Anja M. van der Laan, Hans W. M. Niessen, Jan J. Piek, Barry B. Rubin, Jagdish Butany, James R. Stone, Hugo A. Katus, Sabina A. Murphy, David A. Morrow, Marc S. Sabatine, Claudio Vinegoni, Michael A. Moskowitz, Mikael J. Pittet, Peter Libby, Charles P. Lin, Filip K. Swirski, Ralph Weissleder () and Matthias Nahrendorf ()
Additional contact information
Partha Dutta: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Gabriel Courties: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Ying Wei: Stroke and Neurovascular Regulation Laboratory, Massachusetts General Hospital/Harvard Medical School, 149 13th Street, Charlestown, Massachusetts 02129, USA
Florian Leuschner: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Rostic Gorbatov: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Clinton S. Robbins: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Yoshiko Iwamoto: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Brian Thompson: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Alicia L. Carlson: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Timo Heidt: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Maulik D. Majmudar: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Felix Lasitschka: Institute of Pathology, University Hospital Heidelberg, Im Neuenheimer Feld 220/221, 69120 Heidelberg, Germany
Martin Etzrodt: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Peter Waterman: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Michael T. Waring: The Ragon Institute of MGH, MIT and Harvard at Massachusetts General Hospital
Adam T. Chicoine: The Ragon Institute of MGH, MIT and Harvard at Massachusetts General Hospital
Anja M. van der Laan: Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, the Netherlands
Hans W. M. Niessen: ICaR-VU, VU University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, the Netherlands
Jan J. Piek: Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, the Netherlands
Barry B. Rubin: Peter Munk Cardiac Centre, Toronto General Hospital, University of Toronto, Toronto, Ontario M5G-2C4, Canada
Jagdish Butany: Peter Munk Cardiac Centre, University of Toronto, Toronto, Ontario M5G-2C4, Canada
James R. Stone: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Hugo A. Katus: Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, D-69120 Heidelberg, Germany
Sabina A. Murphy: TIMI Study Group, Brigham and Women’s Hospital
David A. Morrow: TIMI Study Group, Brigham and Women’s Hospital
Marc S. Sabatine: TIMI Study Group, Brigham and Women’s Hospital
Claudio Vinegoni: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Michael A. Moskowitz: Stroke and Neurovascular Regulation Laboratory, Massachusetts General Hospital/Harvard Medical School, 149 13th Street, Charlestown, Massachusetts 02129, USA
Mikael J. Pittet: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Peter Libby: Brigham and Women’s Hospital
Charles P. Lin: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Filip K. Swirski: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Ralph Weissleder: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Matthias Nahrendorf: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA

Nature, 2012, vol. 487, issue 7407, 325-329

Abstract: Abstract During progression of atherosclerosis, myeloid cells destabilize lipid-rich plaques in the arterial wall and cause their rupture, thus triggering myocardial infarction and stroke. Survivors of acute coronary syndromes have a high risk of recurrent events for unknown reasons. Here we show that the systemic response to ischaemic injury aggravates chronic atherosclerosis. After myocardial infarction or stroke, Apoe−/− mice developed larger atherosclerotic lesions with a more advanced morphology. This disease acceleration persisted over many weeks and was associated with markedly increased monocyte recruitment. Seeking the source of surplus monocytes in plaques, we found that myocardial infarction liberated haematopoietic stem and progenitor cells from bone marrow niches via sympathetic nervous system signalling. The progenitors then seeded the spleen, yielding a sustained boost in monocyte production. These observations provide new mechanistic insight into atherogenesis and provide a novel therapeutic opportunity to mitigate disease progression.

Date: 2012
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DOI: 10.1038/nature11260

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