Formyl Peptide Receptor 2 Is Involved in Cardiac Repair After Myocardial Infarction Through Mobilization of Circulating Angiogenic Cells
Autor: | Yang Woo Kwon, Jung Won Yoon, Soon Chul Heo, Tae Wook Lee, Young Keun Ahn, Il Ho Jang, Tae Hee Ko, Geun Ok Jeong, Jae Ho Kim, Sang Chul Lee, Hae Chang Jeong, Ho Jin Shin, Jin Han |
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Rok vydání: | 2016 |
Předmět: |
Male
0301 basic medicine Cardiotonic Agents Myocardial Infarction CD34 Neovascularization Physiologic Bone Marrow Cells 030204 cardiovascular system & hematology Biology Pharmacology Formyl peptide receptor 2 Neovascularization 03 medical and health sciences 0302 clinical medicine medicine Animals Regeneration Myocardial infarction Progenitor cell Endothelial Progenitor Cells Mice Knockout Cell Biology medicine.disease Receptors Formyl Peptide Mice Inbred C57BL Transplantation 030104 developmental biology medicine.anatomical_structure Heart Function Tests Immunology Molecular Medicine Bone marrow Stem cell medicine.symptom Oligopeptides Developmental Biology |
Zdroj: | Stem Cells. 35:654-665 |
ISSN: | 1549-4918 1066-5099 |
Popis: | 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. |
Databáze: | OpenAIRE |
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