Targeting VEGFR1 on endothelial progenitors modulates their differentiation potential View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2014-01-14

AUTHORS

Clément d’Audigier, Benoit Gautier, Alexis Yon, Jean-Meidi Alili, Coralie L. Guérin, Solène M. Evrard, Anne Godier, Skerdi Haviari, Marie Reille-Serroussi, Florent Huguenot, Blandine Dizier, Nicolas Inguimbert, Delphine Borgel, Ivan Bièche, Catherine Boisson-Vidal, Carmen Roncal, Peter Carmeliet, Michel Vidal, Pascale Gaussem, David M. Smadja

ABSTRACT

ObjectivesWe studied whether plasma levels of angiogenic factors VEGF and placental growth factor (PlGF) in coronary artery disease patients or undergoing cardiac surgery are modified, and whether those factors modulate endothelial progenitor’s angiogenic potential.Methods and resultsA total of 143 patients’ plasmas from two different studies were analyzed (30 coronary artery disease patients, 30 patients with stable angina, coupled with 30 age and sex-matched controls; 53 patients underwent cardiac surgery). Among factors screened, only PlGF was found significantly increased in these pathological populations. PlGF-1 and PlGF-2 were then tested on human endothelial-colony-forming cells (ECFCs). We found that PlGF-1 and PlGF-2 induce VEGFR1 phosphorylation and potentiate ECFCs tubulogenesis in vitro. ECFCs VEGFR1 was further inhibited using a specific small interfering RNA (siRNA) and the chemical compound 4321. We then observed that the VEGFR1-siRNA and the compound 4321 decrease ECFCs tubulogenesis potential in vitro. Finally, we tested the compound 4321 in the preclinical Matrigel®-plug model with C57Bl/6J mice as well as in the murine hindlimb ischemia model. We found that 4321 inhibited the plug vascularization, attested by the hemoglobin content and the VE-Cadherin expression level and that 4321 inhibited the post-ischemic revascularization.ConclusionPlGF plasma levels were found increased in cardiovascular patients. Disrupting PlGF/VEGFR1 pathway could modulate ECFC-induced tubulogenesis, the cell type responsible for newly formed vessels in vivo. More... »

PAGES

603-616

Journal

TITLE

Angiogenesis

ISSUE

3

VOLUME

17

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10456-013-9413-2

DOI

http://dx.doi.org/10.1007/s10456-013-9413-2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1019714779

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24419917


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