ArticleJournal of the American College of Cardiology2014
Plasminogen regulates cardiac repair after myocardial infarction through its noncanonical function in stem cell homing to the infarcted heart.
Article in Journal of the American College of Cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 24 citations in OpenAlex.
- Mendelian randomization reveals plasminogen as a common therapeutic target for myocardial infarction and atrial fibrillation.Journal of cardiovascular and thoracic research · 2024Article
- Endothelial plasticity drives aberrant vascularization and impedes cardiac repair after myocardial infarction.Nature cardiovascular research · 2022Article
- Plasminogen Regulates Fracture Repair by Promoting the Functions of Periosteal Mesenchymal Progenitors.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Plasminogen regulates mesenchymal stem cell-mediated tissue repair after ischemia through Cyr61 activation.JCI insight · 2020Article
- Extracellular Matrix in Ischemic Heart Disease, Part 4/4: JACC Focus Seminar.Journal of the American College of Cardiology · 2020Review
- Review
- Interleukin-10 Inhibits Bone Marrow Fibroblast Progenitor Cell-Mediated Cardiac Fibrosis in Pressure-Overloaded Myocardium.Circulation · 2017Article
- Stimulating endogenous cardiac repair.Frontiers in cell and developmental biology · 2015Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesThe purpose of this study was to investigate the role of plasminogen (Plg) in stem cell-mediated cardiac repair and regeneration after myocardial infarction (MI).
backgroundAn MI induces irreversible tissue damage, eventually leading to heart failure. Bone marrow (BM)-derived stem cells promote tissue repair and regeneration after MI. Thrombolytic treatment with Plg activators significantly improves the clinical outcome in MI by restoring cardiac perfusion. However, the role of Plg in stem cell-mediated cardiac repair remains unclear.
methodsAn MI was induced in Plg-deficient (Plg(-/-)) and wild-type (Plg(+/+)) mice by ligation of the left anterior descending coronary artery. Stem cells were visualized by in vivo tracking of green fluorescent protein (GFP)-expressing BM cells after BM transplantation. Cardiac function, stem cell homing, and signaling pathways downstream of Plg were examined.
resultsGranulocyte colony-stimulating factor, a stem cell mobilizer, significantly promoted BM-derived stem cell (GFP(+)c-kit(+) cell) recruitment into the infarcted heart and stem cell-mediated cardiac repair in Plg(+/+) mice. However, Plg deficiency markedly inhibited stem cell homing and cardiac repair, suggesting that Plg is critical for stem cell-mediated cardiac repair. Moreover, Plg regulated C-X-C chemokine receptor type 4 (CXCR4) expression in stem cells in vivo and in vitro through matrix metalloproteinase-9. Lentiviral reconstitution of CXCR4 expression in BM cells successfully rescued stem cell homing to the infarcted heart in Plg-deficient mice, indicating that CXCR4 has a critical role in Plg-mediated stem cell homing after MI.
conclusionsThese findings have identified a novel role for Plg in stem cell-mediated cardiac repair after MI. Thus, targeting Plg may offer a new therapeutic strategy for stem cell-mediated cardiac repair after MI.
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