ArticlePloS one2013
Sustained-release delivery of prostacyclin analogue enhances bone marrow-cell recruitment and yields functional benefits for acute myocardial infarction in mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Regenerative medicine in cardiovascular disease.Regenerative therapy · 2024Review
- Enhanced myocardial blood flow in ischemic cardiomyopathy by a slow-release synthetic prostacyclin agonist combined with coronary artery bypass grafting: The first human study in a Phase I/IIa clinical trial.Frontiers in cardiovascular medicine · 2023Article
- Angiogenic stem cell delivery platform to augment post-infarction neovasculature and reverse ventricular remodeling.Scientific reports · 2022Article
- New regional drug delivery system by direct epicardial placement of slow-release prostacyclin agonist promise therapeutic angiogenesis in a porcine chronic myocardial infarction.Journal of artificial organs : the official journal of the Japanese Society for Artificial Organs · 2021Article
- Combined administration of laminin-221 and prostacyclin agonist enhances endogenous cardiac repair in an acute infarct rat heart.Scientific reports · 2021Article
- Synthetic Prostacyclin Agonist Attenuates Pressure-Overloaded Cardiac Fibrosis by Inhibiting FMT.Molecular therapy. Methods & clinical development · 2020Article
- Administration of Slow-Release Synthetic Prostacyclin Agonist Promoted Angiogenesis and Skeletal Muscle Regeneration for Limb Ischemia.Molecular therapy. Methods & clinical development · 2020Article
- Prostacyclin Analogue-Loaded Nanoparticles Attenuate Myocardial Ischemia/Reperfusion Injury in Rats.JACC. Basic to translational science · 2019Article
- Influence of coronary architecture on the variability in myocardial infarction induced by coronary ligation in rats.PloS one · 2017Article
- Article
- Lidocaine Enhances Contractile Function of Ischemic Myocardial Regions in Mouse Model of Sustained Myocardial Ischemia.PloS one · 2016Article
- A sustained-release drug-delivery system of synthetic prostacyclin agonist, ONO-1301SR: a new reagent to enhance cardiac tissue salvage and/or regeneration in the damaged heart.Heart failure reviews · 2015Review
- Present and future perspectives on cell sheet-based myocardial regeneration therapy.BioMed research international · 2013Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA prostacyclin analogue, ONO-1301, is reported to upregulate beneficial proteins, including stromal cell derived factor-1 (SDF-1). We hypothesized that the sustained-release delivery of ONO-1301 would enhance SDF-1 expression in the acute myocardial infarction (MI) heart and induce bone marrow cells (BMCs) to home to the myocardium, leading to improved cardiac function in mice. METHODS AND
resultsONO-1301 significantly upregulated SDF-1 secretion by fibroblasts. BMC migration was greater to ONO-1301-stimulated than unstimulated conditioned medium. This increase was diminished by treating the BMCs with a CXCR4-neutralizing antibody or CXCR4 antagonist (AMD3100). Atelocollagen sheets containing a sustained-release form of ONO-1301 (n = 33) or ONO-1301-free vehicle (n = 48) were implanted on the left ventricular (LV) anterior wall immediately after permanent left-anterior descending artery occlusion in C57BL6/N mice (male, 8-weeks-old). The SDF-1 expression in the infarct border zone was significantly elevated for 1 month in the ONO-1301-treated group. BMC accumulation in the infarcted hearts, detected by in vivo imaging after intravenous injection of labeled BMCs, was enhanced in the ONO-1301-treated hearts. This increase was inhibited by AMD3100. The accumulated BMCs differentiated into capillary structures. The survival rates and cardiac function were significantly improved in the ONO-1301-treated group (fractional area change 23±1%; n = 22) compared to the vehicle group (19±1%; n = 20; P = 0.004). LV anterior wall thinning, expansion of infarction, and fibrosis were lower in the ONO-1301-treated group.
conclusionsSustained-release delivery of ONO-1301 promoted BMC recruitment to the acute MI heart via SDF-1/CXCR4 signaling and restored cardiac performance, suggesting a novel mechanism for ONO-1301-mediated acute-MI heart repair.
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