Formyl Peptide Receptor 2 Is Involved in Cardiac Repair After Myocardial Infarction Through Mobilization of Circulating Angiogenic Cells. (25th November 2016)

• Record Type: Journal Article
• Authors: Heo, Soon Chul; Kwon, Yang Woo; Jang, Il Ho; Jeong, Geun Ok; Lee, Tae Wook; Yoon, Jung Won; Shin, Ho Jin; Jeong, Hae Chang; Ahn, Youngkeun; Ko, Tae Hee; Lee, Sang Chul; Han, Jin; Kim, Jae Ho
• Is Part Of: Stem cells. Volume 35:Number 3(2017:Mar.)
• Page Start: 654
• Page End: 665
• Publication Date: 2016-11-25
• Subjects: Circulating angiogenic cell -- Formyl peptide receptor -- Mobilization -- Neovascularization -- Myocardial infarction -- WKYMVm; Cloning -- Periodicals; Clone cells -- Periodicals; Stem cells -- Periodicals; Cell Differentiation -- Periodicals; Cell Division -- Periodicals; Clone Cells -- Periodicals; Hematopoietic Stem Cells -- Periodicals; Stem Cells -- Periodicals; 571.84
• DOI: 10.1002/stem.2535
• Languages: English
• ISSNs: 1066-5099

Abstract

Abstract : Increasing evidence suggests that circulating angiogenic cells (CACs) promote repair of ischemic tissues. Activation of formyl peptide receptor 2 (Fpr2) has been reported to stimulate repair of ischemic heart. This study was conducted to investigate the role of Fpr2 on CAC mobilization and cardiac protection in myocardial infarction (MI). WKYMVm, a strong agonist for Fpr2, was administered in a murine model of acute MI, and mobilization of CACs including endothelial progenitor cells (CD34 + Flk1 + or Sca1 + Flk1 + cells) in peripheral blood was monitored. CAC mobilization by daily injection of WKYMVm for the first 4 days after MI was as efficient as granulocyte colony-stimulating factor and provided myocardial protection from apoptosis with increased vascular density and preservation of cardiac function. Transplantation of bone marrow (BM) from green fluorescent protein mice showed that BM-derived cells homed to ischemic heart after WKYMVm treatment and contributed to tissue protection. Transplantation of BM from Fpr2 knockout mice showed that Fpr2 in BM cells is critical in mediation of WKYMVm-stimulated myocardial protection and neovascularization after MI. These results suggest that activation of Fpr2 in BM after WKYMVm treatment provides cardiac protection through mobilization of CACs after MI, which may lead to the development of a new clinical protocol for treating patients with ischemic heart conditions.