Monocyte-Directed RNAi Targeting CCR2 Improves Infarct Healing in Atherosclerosis-Prone Mice | Zendy

Maulik D. Majmudar | Zendy; Edmund J. Keliher | Zendy; Timo Heidt | Zendy; Florian Leuschner | Zendy; Jessica Truelove | Zendy; Brena F. Sena | Zendy; Rostic Gorbatov | Zendy; Yoshiko Iwamoto | Zendy; Partha Dutta | Zendy; Gregory R. Wojtkiewicz | Zendy; Gabriel Courties | Zendy; Matt Sebas | Zendy; Anna Borodovsky | Zendy; Kevin Fitzgerald | Zendy; Marc W. Nolte | Zendy; Gerhard Dickneite | Zendy; John W. Chen | Zendy; Daniel G. Anderson | Zendy; Filip K. Świrski | Zendy; Ralph Weissleder | Zendy; Matthias Nahrendorf | Zendy

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Monocyte-Directed RNAi Targeting CCR2 Improves Infarct Healing in Atherosclerosis-Prone Mice

Author(s) -

Maulik D. Majmudar,

Edmund J. Keliher,

Timo Heidt,

Florian Leuschner,

Jessica Truelove,

Brena F. Sena,

Rostic Gorbatov,

Yoshiko Iwamoto,

Partha Dutta,

Gregory R. Wojtkiewicz,

Gabriel Courties,

Matt Sebas,

Anna Borodovsky,

Kevin Fitzgerald,

Marc W. Nolte,

Gerhard Dickneite,

John W. Chen,

Daniel G. Anderson,

Filip K. Świrski,

Ralph Weissleder,

Matthias Nahrendorf

Publication year - 2013

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.112.000116

Subject(s) - ccr2 , myeloperoxidase , medicine , inflammation , monocyte , gene silencing , positron emission tomography , chemokine , pathology , cancer research , immunology , nuclear medicine , chemokine receptor , chemistry , biochemistry , gene

Exaggerated and prolonged inflammation after myocardial infarction (MI) accelerates left ventricular remodeling. Inflammatory pathways may present a therapeutic target to prevent post-MI heart failure. However, the appropriate magnitude and timing of interventions are largely unknown, in part because noninvasive monitoring tools are lacking. Here, we used nanoparticle-facilitated silencing of CCR2, the chemokine receptor that governs inflammatory Ly-6C(high) monocyte subset traffic, to reduce infarct inflammation in apolipoprotein E-deficient (apoE(-/-)) mice after MI. We used dual-target positron emission tomography/magnetic resonance imaging of transglutaminase factor XIII (FXIII) and myeloperoxidase (MPO) activity to monitor how monocyte subset-targeted RNAi altered infarct inflammation and healing.

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