Injectable human recombinant collagen matrices limit adverse remodeling and improve cardiac function after myocardial infarction

Sarah McLaughlin, Brian McNeill, James Podrebarac, Katsuhiro Hosoyama, Veronika Sedlakova, Gregory Cron, David Smyth, Richard Seymour, Keshav Goel, Wenbin Liang, Katey J. Rayner, Marc Ruel, Erik J. Suuronen () and Emilio I. Alarcon ()
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Sarah McLaughlin: University of Ottawa Heart Institute
Brian McNeill: University of Ottawa Heart Institute
James Podrebarac: University of Ottawa Heart Institute
Katsuhiro Hosoyama: University of Ottawa Heart Institute
Veronika Sedlakova: University of Ottawa Heart Institute
Gregory Cron: University of Ottawa
David Smyth: University of Ottawa Heart Institute
Richard Seymour: University of Ottawa Heart Institute
Keshav Goel: University of Ottawa Heart Institute
Wenbin Liang: University of Ottawa
Katey J. Rayner: University of Ottawa Heart Institute
Marc Ruel: University of Ottawa Heart Institute
Erik J. Suuronen: University of Ottawa Heart Institute
Emilio I. Alarcon: University of Ottawa Heart Institute

Nature Communications, 2019, vol. 10, issue 1, 1-14

Abstract: Abstract Despite the success of current therapies for acute myocardial infarction (MI), many patients still develop adverse cardiac remodeling and heart failure. With the growing prevalence of heart failure, a new therapy is needed that can prevent remodeling and support tissue repair. Herein, we report on injectable recombinant human collagen type I (rHCI) and type III (rHCIII) matrices for treating MI. Injecting rHCI or rHCIII matrices in mice during the late proliferative phase post-MI restores the myocardium’s mechanical properties and reduces scar size, but only the rHCI matrix maintains remote wall thickness and prevents heart enlargement. rHCI treatment increases cardiomyocyte and capillary numbers in the border zone and the presence of pro-wound healing macrophages in the ischemic area, while reducing the overall recruitment of bone marrow monocytes. Our findings show functional recovery post-MI using rHCI by promoting a healing environment, cardiomyocyte survival, and less pathological remodeling of the myocardium.

Date: 2019
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-12748-8

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DOI: 10.1038/s41467-019-12748-8

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