ArticleThe Journal of experimental medicine2004
Down-regulation of plasminogen activator inhibitor 1 expression promotes myocardial neovascularization by bone marrow progenitors.
Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 40 citations in OpenAlex.
- A promising nucleic acid therapy drug: DNAzymes and its delivery system.Frontiers in molecular biosciences · 2023Review
- Transforming growth factor-β1/Thrombospondin-1/CD47 axis mediates dysfunction in CD34European journal of pharmacology · 2022Article
- Enhancing the function of CD34(+) cells by targeting plasminogen activator inhibitor-1.PloS one · 2013Article
- A phenomics-based strategy identifies loci on APOC1, BRAP, and PLCG1 associated with metabolic syndrome phenotype domains.PLoS genetics · 2011Article
- Sonic hedgehog-induced functional recovery after myocardial infarction is enhanced by AMD3100-mediated progenitor-cell mobilization.Journal of the American College of Cardiology · 2011Article
- Deoxyribozymes: new therapeutics to treat central nervous system disorders.Frontiers in molecular neuroscience · 2011Article
- Role of endothelial progenitor cells during ischemia-induced vasculogenesis and collateral formation.Microvascular research · 2010Review
- Metabolic syndrome and collateral vessel formation in patients with documented occluded coronary arteries: association with hyperglycaemia, insulin-resistance, adiponectin and plasminogen activator inhibitor-1.European heart journal · 2009Article
- Features of cardiomyocyte proliferation and its potential for cardiac regeneration.Journal of cellular and molecular medicine · 2008Review
- Genetic enhancement of stem cell engraftment, survival, and efficacy.Circulation research · 2008Review
- DNAzymes and cardiovascular disease.British journal of pharmacology · 2008Review
- Brothers in arms: DNA enzymes, short interfering RNA, and the emerging wave of small-molecule nucleic acid-based gene-silencing strategies.The American journal of pathology · 2007Review
- Managing drugs and devices in patients with permanent ventricular assist devices.Current treatment options in cardiovascular medicine · 2007Article
- Biomarkers of obesity and subsequent cardiovascular events.Epidemiologic reviews · 2007Review
- Engraftment of engineered ES cell-derived cardiomyocytes but not BM cells restores contractile function to the infarcted myocardium.The Journal of experimental medicine · 2006Article
- In vitro selection, characterization, and application of deoxyribozymes that cleave RNA.Nucleic acids research · 2005Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Human adult bone marrow-derived endothelial progenitors, or angioblasts, induce neovascularization of infarcted myocardium via mechanisms involving both cell surface urokinase-type plasminogen activator, and interactions between beta integrins and tissue vitronectin. Because each of these processes is regulated by plasminogen activator inhibitor (PAI)-1, we selectively down-regulated PAI-1 mRNA in the adult heart to examine the effects on postinfarct neovascularization and myocardial function. Sequence-specific catalytic DNA enzymes inhibited rat PAI-1 mRNA and protein expression in peri-infarct endothelium within 48 h of administration, and maintained down-regulation for at least 2 wk. PAI-1 inhibition enhanced vitronectin-dependent transendothelial migration of human bone marrow-derived CD34+ cells, and resulted in a striking augmentation of angioblast-dependent neovascularization. Development of large, thin-walled vessels at the peri-infarct region was accompanied by induction of proliferation and regeneration of endogenous cardiomyocytes and functional cardiac recovery. These results identify a causal relationship between elevated PAI-1 levels and poor outcome in patients with myocardial infarction through mechanisms that directly inhibit bone marrow-dependent neovascularization. Strategies that reduce myocardial PAI-1 expression appear capable of enhancing cardiac neovascularization, regeneration, and functional recovery after ischemic insult.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.