ArticlePloS one2012
Tie2-dependent neovascularization of the ischemic hindlimb is mediated by angiopoietin-2.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Tie2 Receptor in Tumor-Infiltrating Macrophages Is Dispensable for Tumor Angiogenesis and Tumor Relapse after Chemotherapy.Cancer research · 2022Pooled it
- Modulation of miR-29a and ADAM12 Reduces Post-Ischemic Skeletal Muscle Injury and Improves Perfusion Recovery and Skeletal Muscle Function in a Mouse Model of Type 2 Diabetes and Peripheral Artery Disease.International journal of molecular sciences · 2021Article
- New Directions in Therapeutic Angiogenesis and Arteriogenesis in Peripheral Arterial Disease.Circulation research · 2021Review
- Prognostic Value of Tie2-Expressing Monocytes in Chronic Lymphocytic Leukemia Patients.Cancers · 2021Article
- Vascular Regeneration in Peripheral Artery Disease.Arteriosclerosis, thrombosis, and vascular biology · 2020Review
- Myeloid ALX/FPR2 regulates vascularization following tissue injury.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- miR-15a/-16 Inhibit Angiogenesis by Targeting the Tie2 Coding Sequence: Therapeutic Potential of a miR-15a/16 Decoy System in Limb Ischemia.Molecular therapy. Nucleic acids · 2019Article
- Vascular leakage caused by loss of Akt1 is associated with impaired mural cell coverage.FEBS open bio · 2019Article
- Article
- A Review of Anti-Angiogenic Targets for Monoclonal Antibody Cancer Therapy.International journal of molecular sciences · 2017Review
- Angiopoietin-2 impairs collateral artery growth associated with the suppression of the infiltration of macrophages in mouse hindlimb ischaemia.Journal of translational medicine · 2016Article
- Neovascularization Potential of Blood Outgrowth Endothelial Cells From Patients With Stable Ischemic Heart Failure Is Preserved.Journal of the American Heart Association · 2016Article
- ADAM12: a genetic modifier of preclinical peripheral arterial disease.American journal of physiology. Heart and circulatory physiology · 2015Article
- Article
- PHD2 regulates arteriogenic macrophages through TIE2 signalling.EMBO molecular medicine · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The angiopoietins (ANGPT) are ligands for the endothelial cell (EC) receptor tyrosine kinase, Tie2. Angpt-1 is a Tie2 agonist that promotes vascular maturation and stabilization, whereas Angpt-2 is a partial agonist/antagonist involved in the initiation of postnatal angiogenesis. Therefore, we hypothesized that overexpression of Angpt-2 would be more effective than Angpt-1 for enhancing the perfusion recovery in the ischemic hindlimb. Perfusion recovery was markedly impaired in Tie2-deficient animals at day 35 in a model of chronic hindlimb ischemia. Injections of Angpt-2 or VEGFA plasmid at 7 days post femoral artery resection enhanced recovery and improved arteriogenesis as assessed by angiographic scores, whereas Angpt-1 or null plasmid had no effect. In addition, Angpt-2 together with VEGF resulted in greater improvement in perfusion and collateral vessel formation than VEGF alone. Similarly, conditional overexpression of Angpt-2 in mice improved ischemic limb blood flow recovery, while Angpt-1 overexpression was ineffective. These data from Tie2 heterozygote deficient mice demonstrate, for the first time, the importance of the Tie2 pathway in spontaneous neovascularization in response to chronic hindlimb ischemia. Moreover, they show that overexpression of the partial agonist, Angpt-2, but not Angpt-1, enhanced ischemic hind limb perfusion recovery and collateralization, suggesting that a coordinated sequence antagonist and agonist activity is required for effective therapeutic revascularization.
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