Apelin Enhances Cardiac Neovascularization After Myocardial Infarction by Recruiting Aplnr plus Circulating Cells

Dennie Tempel, MF de Boer, Elza Deel, Remco Haasdijk, Dirk-jan Duncker, Caroline Cheng, S Schulte-Merker, Eric Duckers

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Rationale: Neovascularization stimulated by local or recruited stem cells after ischemia is a key process that salvages damaged tissue and shows similarities with embryonic vascularization. Apelin receptor (Aplnr) and its endogenous ligand apelin play an important role in cardiovascular development. However, the role of apelin signaling in stem cell recruitment after ischemia is unknown. Objective: To investigate the role of apelin signaling in recruitment after ischemia. Methods and Results: Aplnr was specifically expressed in circulating cKit+/Flk1+ cells but not in circulating Sca1+/Flk1+ and Lin+ cells. cKit+/Flk1+/Aplnr+ cells increased significantly early after myocardial ischemia but not after hind limb ischemia, indicative of an important role for apelin/Aplnr in cell recruitment during the nascent biological repair response after myocardial damage. In line with this finding, apelin expression was upregulated in the infarcted myocardium. Injection of apel Conclusions: We conclude that apelin functions as a new and potent chemoattractant for circulating cKit+/Flk1+/Aplnr+ cells during early myocardial repair, providing myocardial protection against ischemic damage by improving neovascularization via paracine action. (Circ Res. 2012;111:585-598.)
Original languageUndefined/Unknown
Pages (from-to)585-U327
JournalCirculation Research
Issue number5
Publication statusPublished - 2012

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