ArticleBritish journal of pharmacology2008
ATL-1, an analogue of aspirin-triggered lipoxin A4, is a potent inhibitor of several steps in angiogenesis induced by vascular endothelial growth factor.
Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 64 citations in OpenAlex.
- G protein-coupled receptors and inflammation resolution signaling networks in the heart: Pharmacology and potential for innovative therapeutics.Pharmacological reviews · 2026Review
- Lipoxins as Modulators of Diseases.Cells · 2025Review
- Aspirin-triggered DHA metabolites inhibit angiogenesis.Frontiers in pharmacology · 2025Article
- Atractylenolide I inhibits EMT and enhances the antitumor effect of cabozantinib in prostate cancerFrontiers in oncology · 2022Article
- Carcinogenesis: Failure of resolution of inflammation?Pharmacology & therapeutics · 2021Review
- Signal Pathways and Markers Involved in Acute Lung Injury Induced by Acute Pancreatitis.Disease markers · 2021Review
- Simvastatin Improves Cardiac Function through Notch 1 Activation in BALB/c Mice with Chronic Chagas Cardiomyopathy.Antimicrobial agents and chemotherapy · 2020Article
- Molecular Targets of Aspirin and Prevention of Preeclampsia and Their Potential Association with Circulating Extracellular Vesicles during Pregnancy.International journal of molecular sciences · 2019Review
- Identification and structure elucidation of the pro-resolving mediators provides novel leads for resolution pharmacology.British journal of pharmacology · 2019Review
- Crotoxin promotes macrophage reprogramming towards an antiangiogenic phenotype.Scientific reports · 2019Article
- Walker 256 Tumor Growth Suppression by Crotoxin Involves Formyl Peptide Receptors and Lipoxin A₄.Mediators of inflammation · 2016Article
- Lipoxin A4 suppresses the development of endometriosis in an ALX receptor-dependent manner via the p38 MAPK pathway.British journal of pharmacology · 2014Article
- Aspirin modulates innate inflammatory response and inhibits the entry of Trypanosoma cruzi in mouse peritoneal macrophages.Mediators of inflammation · 2014Article
- Molecular mechanism of the inhibition effect of Lipoxin A4 on corneal dissolving pathology process.International journal of ophthalmology · 2013Article
- A lipoxin A4 analog ameliorates blood-brain barrier dysfunction and reduces MMP-9 expression in a rat model of focal cerebral ischemia-reperfusion injury.Journal of molecular neuroscience : MN · 2012Article
- Cyclooxygenases and lipoxygenases in cancer.Cancer metastasis reviews · 2011Review
- Inhibition of aldose reductase prevents angiogenesis in vitro and in vivo.Angiogenesis · 2011Article
- Resolvins: natural agonists for resolution of pulmonary inflammation.Progress in lipid research · 2011Review
- Endogenous LXA4 circuits are determinants of pathological angiogenesis in response to chronic injury.The American journal of pathology · 2010Article
- Resolvins and protectins: mediating solutions to inflammation.British journal of pharmacology · 2009Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeVascular endothelial growth factor (VEGF) is the most important proangiogenic protein. We have demonstrated that ATL-1, a synthetic analogue of aspirin-triggered lipoxin A(4), inhibits VEGF-induced endothelial cell (EC) migration. In the present study, we investigated the effects of ATL-1 in several other actions stimulated by VEGF.
methodsHuman umbilical vein ECs were treated with ATL-1 for 30 min before stimulation with VEGF. Cell proliferation was measured by thymidine incorporation. Adherent cells were determined by fluorescence intensity using a Multilabel counter. Expression and activity of matrix metalloproteinases (MMP) were analysed by western blot and zymography. KEY
resultsATL-1 inhibited EC adhesion to fibronectin via interaction with its specific receptor. Furthermore, VEGF-induced MMP-9 activity and expression were reduced by pretreatment with ATL-1. Because the transcription factor NF-kappaB has been implicated in VEGF-mediated MMP expression and EC proliferation, we postulated that ATL-1 might modulate the NF-kappaB pathway and, indeed, ATL-1 inhibited NF-kappaB nuclear translocation. Pretreatment of EC with ATL-1 strongly decreased VEGF-dependent phosphorylation of phosphainositide 3-kinase (PI3-K) and extracellular signal-regulated kinase-2 (ERK-2), two signalling kinases involved in EC proliferation. Inhibition of VEGF-induced EC proliferation by ATL-1 was antagonized by sodium orthovanadate, suggesting that this inhibitory activity was mediated by a protein tyrosine phosphatase. This was confirmed by showing that ATL-1 inhibition of VEGF receptor-2 (VEGFR-2) phosphorylation correlates with SHP-1 association with VEGFR-2. CONCLUSIONS AND IMPLICATIONS: The synthetic 15-epi-lipoxin analogue, ATL-1, is a highly potent molecule exerting its effects on multiple steps of the VEGF-induced angiogenesis.
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