Sung-Whan Kim1, Hong Lian Jin2, Seok-Min Kang3, Sinyoung Kim4, Kyung-Jong Yoo5, Yangsoo Jang2, Hyun Ok Kim6, Young-sup Yoon7. 1. Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA; Department of Medicine, College of Medicine, Catholic Kwandong University, Gangneung, Republic of Korea. 2. Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Republic of Korea. 3. Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea. 4. Department of Laboratory Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea. 5. Department of Cardiovascular Surgery, Yonsei University College of Medicine, Seoul, Republic of Korea. 6. Department of Laboratory Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea. Electronic address: Hyunok1019@yuhs.ac. 7. Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA; Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Republic of Korea. Electronic address: yyoon5@emory.edu.
Abstract
BACKGROUND: This study sought to systematically investigate the derivation of late outgrowth endothelial progenitor cells (late EPC) and mesenchymal stem cells (MSC) from umbilical cord blood (UCB) and to examine their therapeutic effects on myocardial infarction (MI). METHODS: The expression of angiogenic genes was determined by qRT-PCR. Myocardial infarction (MI) was induced in rats, and cells were directly transplanted into the border regions of ischemic heart tissue. RESULTS: Culture of UCB mononuclear cells yielded two distinct types of cells by morphology after 2 weeks in the same culture conditions. These cells were identified as late EPC and MSC, and each was intramyocardially injected into rat hearts after induction of MI. Echocardiography and histologic analyses demonstrated that both EPC and MSC improved cardiac function and enhanced vascularization, although fibrosis was reduced only in the EPC transplanted hearts. Different paracrine factors were enriched in EPC and MSC. However, once injected into the hearts, they induced similar types of paracrine factors in the heart. Transplanted EPC or MSC were mostly localized at the perivascular areas. This study demonstrated that EPC and MSC can be simultaneously derived from UCB under the same initial culture conditions, and that common paracrine factors are involved in the repair of MI. CONCLUSION: Late EPC and MSC are effective for infarct repair, apparently mediated through common humoral mechanisms.
BACKGROUND: This study sought to systematically investigate the derivation of late outgrowth endothelial progenitor cells (late EPC) and mesenchymal stem cells (MSC) from umbilical cord blood (UCB) and to examine their therapeutic effects on myocardial infarction (MI). METHODS: The expression of angiogenic genes was determined by qRT-PCR. Myocardial infarction (MI) was induced in rats, and cells were directly transplanted into the border regions of ischemic heart tissue. RESULTS: Culture of UCB mononuclear cells yielded two distinct types of cells by morphology after 2 weeks in the same culture conditions. These cells were identified as late EPC and MSC, and each was intramyocardially injected into rat hearts after induction of MI. Echocardiography and histologic analyses demonstrated that both EPC and MSC improved cardiac function and enhanced vascularization, although fibrosis was reduced only in the EPC transplanted hearts. Different paracrine factors were enriched in EPC and MSC. However, once injected into the hearts, they induced similar types of paracrine factors in the heart. Transplanted EPC or MSC were mostly localized at the perivascular areas. This study demonstrated that EPC and MSC can be simultaneously derived from UCB under the same initial culture conditions, and that common paracrine factors are involved in the repair of MI. CONCLUSION: Late EPC and MSC are effective for infarct repair, apparently mediated through common humoral mechanisms.
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