Abstract
Angiogenesis is a mechanism that has repercussions in a number of physiological and pathological situations. Vascular endothelial growth factor and basic fibroblast growth factor have understandably received enormous research coverage for being the major mediators of new blood vessel growth, often overshadowing other agonist that also have strong angiogenic potential. We wish to put the spotlight on GPCR agonists that undoubtedly have their word to say on the subject of angiogenesis. In this short review, we will discuss our findings along with the work from other groups on the mechanisms by which GPCR agonists, like thrombin and angiotensin II, control a number of angiogenic signals. A complete understanding of these mechanisms could, by the design of new therapeutic strategies, have a strong impact in clinical oncology.
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Abbreviations
- Ang II:
-
Angiotensin II
- GPCR:
-
G-protein coupled receptor
- HIF:
-
Hypoxia Inducible Factor
- HUVEC:
-
Human Umbilical Vein Endothelial Cells
- ROS:
-
Reactive Oxygen Species
- VEGF:
-
Vascular Endothelial Growth Factor
- pVHL:
-
von Hippel-Lindau protein complex
- VSMC:
-
Vascular Smooth Muscle Cells.
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Acknowledgements
The authors wish to thank Dr Edurne Berra for her critical reading of the manuscript. DE Richard is a recipient of a Fellowship from the Canadian Institutes of Health Research (CIHR). This work was supported by grants from the Centre National de la Recherche Scientifique (CNRS), the University of Nice, La Ligue Nationale Contre le Cancer (Equipe labellisée), and the GIP HMR contract.
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Richard, D., Vouret-Craviari, V. & Pouysségur, J. Angiogenesis and G-protein-coupled receptors: signals that bridge the gap. Oncogene 20, 1556–1562 (2001). https://doi.org/10.1038/sj.onc.1204193
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DOI: https://doi.org/10.1038/sj.onc.1204193
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