Formyl Peptide Receptor 2 Is Involved in Cardiac Repair After Myocardial Infarction Through Mobilization of Circulating Angiogenic Cells
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. S tem C ells 2017;35:654–665 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. Administration of WKYMVm induced mobilization of CACs in peripheral blood in a murine model of acute myocardial infarction through Fpr2‐dependent mechanism. CAC mobilization provided myocardial protection from apoptosis with increased vascular density and preservation of cardiac function. These results suggest that activation of Fpr2 in bone marrow after WKYMVm treatment provides cardiac protection through mobilization of CACs after myocardial infarction, which may lead to the development of a new clinical protocol for treating patients with ischemic heart conditions..
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2017 |
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| Erschienen: |
2017 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:35 |
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| Enthalten in: |
Stem cells - 35(2017), 3, Seite 654-665 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Heo, Soon Chul [VerfasserIn] |
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| Themen: |
Circulating angiogenic cell |
| doi: |
10.1002/stem.2535 |
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| 520 | |a 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. S tem C ells 2017;35:654–665 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. Administration of WKYMVm induced mobilization of CACs in peripheral blood in a murine model of acute myocardial infarction through Fpr2‐dependent mechanism. CAC mobilization provided myocardial protection from apoptosis with increased vascular density and preservation of cardiac function. These results suggest that activation of Fpr2 in bone marrow after WKYMVm treatment provides cardiac protection through mobilization of CACs after myocardial infarction, which may lead to the development of a new clinical protocol for treating patients with ischemic heart conditions. | ||
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