ArticleCardiovascular research2016
Genetic lineage tracing discloses arteriogenesis as the main mechanism for collateral growth in the mouse heart.
Article in Cardiovascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 51 citations in OpenAlex.
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- Development of pial collaterals by extension of pre-existing artery tips.Cell reports · 2024Article
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- Coronary vessels contribute to de novo endocardial cells in the endocardium-depleted heart.Cell discovery · 2023Article
- Tubular Elabela-APJ axis attenuates ischemia-reperfusion induced acute kidney injury and the following AKI-CKD transition by protecting renal microcirculation.Theranostics · 2023Article
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- Computational insights on coronary artery function.Nature cardiovascular research · 2022Article
- Blood flow modeling reveals improved collateral artery performance during the regenerative period in mammalian hearts.Nature cardiovascular research · 2022Article
- The essential role for endothelial cell sprouting in coronary collateral growth.Journal of molecular and cellular cardiology · 2022Article
- Heterogeneity in endothelial cells and widespread venous arterialization during early vascular development in mammals.Cell research · 2022Article
- Formation and Maintenance of the Natural Bypass Vessels of the Brain.Frontiers in cardiovascular medicine · 2022Review
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- Setd4 controlled quiescent c-KitScientific reports · 2021Article
- Review
- New Research Is Shining Light on How Collateral Arteries Form in the Heart: a Future Therapeutic Direction?Current cardiology reports · 2021Review
- Structural Remodeling of the Extracellular Matrix in Arteriogenesis: A Review.Frontiers in cardiovascular medicine · 2021Review
- Decreased inspired oxygen stimulates de novo formation of coronary collaterals in adult heart.Journal of molecular and cellular cardiology · 2021Article
- Genetic lineage tracing reveals poor angiogenic potential of cardiac endothelial cells.Cardiovascular research · 2021Article
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsCapillary and arterial endothelial cells share many common molecular markers in both the neonatal and adult hearts. Herein, we aim to establish a genetic tool that distinguishes these two types of vessels in order to determine the cellular mechanism underlying collateral artery formation. METHODS AND
resultsUsing Apln-GFP and Apln-LacZ reporter mice, we demonstrate that APLN expression is enriched in coronary vascular endothelial cells. However, APLN expression is reduced in coronary arterial endothelial cells. Genetic lineage tracing, using an Apln-CreER mouse line, robustly labelled capillary endothelial cells, but not arterial endothelial cells. We leveraged this differential activity of Apln-CreER to study collateral artery formation following myocardial infarction (MI). In a neonatal heart MI model, we found that Apln-CreER-labelled capillary endothelial cells do not contribute to the large collateral arteries. Instead, these large collateral arteries mainly arise from pre-existing, infrequently labelled coronary arteries, indicative of arteriogenesis. Furthermore, in an adult heart MI model, Apln-CreER activity also distinguishes large and small diameter arteries from capillaries. Lineage tracing in this setting demonstrated that most large and small coronary arteries in the infarcted myocardium and border region are derived not from capillaries, but from pre-existing arteries.
conclusionApln-CreER-mediated lineage tracing distinguishes capillaries from large arteries, in both the neonatal and adult hearts. Through genetic fate mapping, we demonstrate that pre-existing arteries, but not capillaries, extensively contribute to collateral artery formation following myocardial injury. These results suggest that arteriogenesis is the major mechanism underlying collateral vessel formation.
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