Spatiotemporal control of neutrophil fate to tune inflammation and repair for myocardial infarction therapy

Cheesue Kim, Hyeok Kim, Woo-Sup Sim, Mungyo Jung, Jihye Hong, Sangjun Moon, Jae-Hyun Park, Jin-Ju Kim, Mikyung Kang, Sungpil Kwon, Mi-Jeong Kim, Kiwon Ban, Hun-Jun Park () and Byung‐Soo Kim ()
Additional contact information
Cheesue Kim: Seoul National University
Hyeok Kim: The Catholic University of Korea
Woo-Sup Sim: The Catholic University of Korea
Mungyo Jung: Seoul National University
Jihye Hong: Seoul National University
Sangjun Moon: Seoul National University
Jae-Hyun Park: The Catholic University of Korea
Jin-Ju Kim: The Catholic University of Korea
Mikyung Kang: Korea University
Sungpil Kwon: Seoul National University
Mi-Jeong Kim: Seoul Saint Mary’s Hospital
Kiwon Ban: City University of Hong Kong
Hun-Jun Park: The Catholic University of Korea
Byung‐Soo Kim: Seoul National University

Nature Communications, 2024, vol. 15, issue 1, 1-19

Abstract: Abstract Neutrophils are critical mediators of both the initiation and resolution of inflammation after myocardial infarction (MI). Overexuberant neutrophil signaling after MI exacerbates cardiomyocyte apoptosis and cardiac remodeling while neutrophil apoptosis at the injury site promotes macrophage polarization toward a pro-resolving phenotype. Here, we describe a nanoparticle that provides spatiotemporal control over neutrophil fate to both stymie MI pathogenesis and promote healing. Intravenous injection of roscovitine/catalase-loaded poly(lactic-co-glycolic acid) nanoparticles after MI leads to nanoparticle uptake by circulating neutrophils migrating to the infarcted heart. Activated neutrophils at the infarcted heart generate reactive oxygen species, triggering intracellular release of roscovitine, a cyclin-dependent kinase inhibitor, from the nanoparticles, thereby inducing neutrophil apoptosis. Timely apoptosis of activated neutrophils at the infarcted heart limits neutrophil-driven inflammation, promotes macrophage polarization toward a pro-resolving phenotype, and preserves heart function. Modulating neutrophil fate to tune both inflammatory and reparatory processes may be an effective strategy to treat MI.

Date: 2024
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DOI: 10.1038/s41467-024-52812-6

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