Prokineticin Receptor-1 Signaling Inhibits Dose- and Time-Dependent Anthracycline-Induced Cardiovascular Toxicity Via Myocardial and Vascular Protection.
Fiche publication
Date publication
septembre 2019
Journal
JACC. CardioOncology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr DESAUBRY Laurent
Tous les auteurs :
Gasser A, Chen YW, Audebrand A, Daglayan A, Charavin M, Escoubet B, Karpov P, Tetko I, Chan MWY, Cardinale D, Désaubry L, Nebigil CG
Lien Pubmed
Résumé
This study investigated how different concentrations of doxorubicin (DOX) can affect the function of cardiac cells. This study also examined whether activation of prokineticin receptor (PKR)-1 by a nonpeptide agonist, IS20, prevents DOX-induced cardiovascular toxicity in mouse models.
Mots clés
DMSO, dimethyl sulfoxide, EC, endothelial cell, EDPC, epicardium-derived progenitor cell, EF, ejection fraction, FS, fractional shortening, GPCR, G-protein–coupled receptor, HAEC, human aortic endothelial cell, HF, heart failure, HFrEF, heart failure with reduced ejection fraction, MAPK, mitogen-activated protein kinase, NRF2, nuclear factor, erythroid 2 like 2 (also known as NFE2L2), PECAM, platelet and endothelial cell adhesion molecule, PKR1, prokineticin receptor-1 (also known as PROKR1), PKR1-KO, prokineticin receptor 1 knockout mice, PROK1, prokineticin 1, PROK2, prokineticin 2, TUNEL, terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling, breast cancer, doxorubicin, endothelial dysfunction, epicardial progenitor cells, heart failure
Référence
JACC CardioOncol. 2019 Sep;1(1):84-102