作者: Hiroto Iwasaki , Atsuhiko Kawamoto , Masakazu Ishikawa , Akira Oyamada , Shuko Nakamori
DOI: 10.1161/CIRCULATIONAHA.105.541268
关键词:
摘要: Background— Multilineage developmental capacity of the CD34+ cells, especially into cardiomyocytes and smooth muscle cells (SMCs), is still controversial. In present study we performed a series experiments to prove our hypothesis that vasculogenesis cardiomyogenesis after myocardial infarction (MI) may be dose-dependently enhanced cell transplantation. Methods Results— Peripheral blood were isolated from total mononuclear patients with limb ischemia by apheresis 5-day administration granulocyte colony-stimulating factor. PBS 1×103 (low), 1×105 (mid), or 5×105 (high) intramyocardially transplanted ligation left anterior descending coronary artery nude rats. Functional assessments use echocardiography microtip conductance catheter at day 28 revealed dose-dependent preservation ventricular function transplantation. Necropsy examination disclosed augmentation capillary density inhibition fibrosis. Immunohistochemistry for human-specific brain natriuretic peptide demonstrated human observed in ischemic myocardium (high, 2480±149; mid, 1860±141; low, 423±9; PBS, 0±0/mm2; P <0.05 high versus mid low). Immunostaining actin leukocyte antigen Ulex europaeus lectin type 1 also endothelial SMC development Reverse transcriptase–polymerase chain reaction indicated gene expression cardiomyocyte (brain peptide, cardiac troponin-I, myosin heavy chain, Nkx 2.5), (smooth sm22α), (CD31 KDR) markers augmented MI tissue. Conclusions— Human transplantation have significant potential functional recovery MI. Received February 8, 2005; revision received August 2, accepted September 13, 2005.