This study was designed to determine the levels of early endothelial progenitor cells （EPCs）, apelin, vascu- lar endothelial growth factor （VEGF） and stromal cell-derived growth factor-1 （SDF-1） after acute myoc...This study was designed to determine the levels of early endothelial progenitor cells （EPCs）, apelin, vascu- lar endothelial growth factor （VEGF） and stromal cell-derived growth factor-1 （SDF-1） after acute myocardial infarction （AMI）, and to investigate the relationships between these cytokines and early EPCs. Early EPCs, de- fined as CD133＋, KDR＋, and CD34~ cells, were quantified by flow cytometry. The levels of early EPCs and those cytokines in AMI patients were significantly different from those with coronary artery disease or controls （P 〈 0.05）. Plasma apelin levels were inversely correlated with Gensini score and early EPCs （both P 〈 0.01）. Early EPCs, VEGF and SDF-1 showed different patterns of changes in AMI patients during the first 24 h. The trend in the change of early EPCs was proportionally correlated with that of VEGF （P 〈 0.05）. AMI patients exhibited in- creased early EPCs with remarkably decreased apelin levels and enhanced VEGF levels.展开更多
Endothelial progenitor cells （EPCs） participate in the processes of postnatal neovascularization and re-endothelialization in response to tissue ischemia and endothelial injury. The level of EPCs present has been fo...Endothelial progenitor cells （EPCs） participate in the processes of postnatal neovascularization and re-endothelialization in response to tissue ischemia and endothelial injury. The level of EPCs present has been found to be directly associated with the outcome of cardiovascular diseases, and could be regulated by stimulatory or inhibitory factors. Given the close relationship between angiotensin Ⅱ （AngⅡ） and the cardiovascular＇ system, we investigated the effect of AngⅡ on the activities of bone marrow （BM）-derived EPCs. Cells were isolated from BM of rats by density gradient centrifugation. Administration of AngⅡ significantly promoted nitric oxide （NO） release, inhibited EPC apoptosis and enhanced EPC adhesion potential. All of these AngⅡ-mediated effects on EPCs were attenuated by pretreatment with valsartan or L-NAME. Moreover, both LY294002 and wortmannin abolished the anti-apoptotic effect of AngⅡ. Western blot analyses indicated that endothelial NO synthase （eNOS） protein and phosphorylated Akt increased with the treatment of AngⅡ in EPCs. Thus, AngⅡ improved several activities of EPCs through AngⅡ type 1 receptor （AT1R）, which may represent a possible mechanism linking AnglI and ATIR with angiogenesis. Additionally, AngⅡ-induced NO synthesis through eNOS in EPCs regulates apoptosis and adhesion, and the PI3-kinase/Akt pathway has an essential role in AngⅡ-induced antiapoptosis signaling.展开更多
基金supported by the program (No. CX10B_421Z to Jiaxin Ye) for Postgraduate Research Innovation in Universities of Jiangsu Provincethe grants (No. 81070195) and (No. 81000055) from Chinese National Science Fund of China (all to Biao Xu)grant (No.KF200938 to Lina Kang) from Jiangsu Province
文摘This study was designed to determine the levels of early endothelial progenitor cells （EPCs）, apelin, vascu- lar endothelial growth factor （VEGF） and stromal cell-derived growth factor-1 （SDF-1） after acute myocardial infarction （AMI）, and to investigate the relationships between these cytokines and early EPCs. Early EPCs, de- fined as CD133＋, KDR＋, and CD34~ cells, were quantified by flow cytometry. The levels of early EPCs and those cytokines in AMI patients were significantly different from those with coronary artery disease or controls （P 〈 0.05）. Plasma apelin levels were inversely correlated with Gensini score and early EPCs （both P 〈 0.01）. Early EPCs, VEGF and SDF-1 showed different patterns of changes in AMI patients during the first 24 h. The trend in the change of early EPCs was proportionally correlated with that of VEGF （P 〈 0.05）. AMI patients exhibited in- creased early EPCs with remarkably decreased apelin levels and enhanced VEGF levels.
基金Acknowledgments This work was supported by the National Natural Science Foundation of China （No. 30370581）.
文摘Endothelial progenitor cells （EPCs） participate in the processes of postnatal neovascularization and re-endothelialization in response to tissue ischemia and endothelial injury. The level of EPCs present has been found to be directly associated with the outcome of cardiovascular diseases, and could be regulated by stimulatory or inhibitory factors. Given the close relationship between angiotensin Ⅱ （AngⅡ） and the cardiovascular＇ system, we investigated the effect of AngⅡ on the activities of bone marrow （BM）-derived EPCs. Cells were isolated from BM of rats by density gradient centrifugation. Administration of AngⅡ significantly promoted nitric oxide （NO） release, inhibited EPC apoptosis and enhanced EPC adhesion potential. All of these AngⅡ-mediated effects on EPCs were attenuated by pretreatment with valsartan or L-NAME. Moreover, both LY294002 and wortmannin abolished the anti-apoptotic effect of AngⅡ. Western blot analyses indicated that endothelial NO synthase （eNOS） protein and phosphorylated Akt increased with the treatment of AngⅡ in EPCs. Thus, AngⅡ improved several activities of EPCs through AngⅡ type 1 receptor （AT1R）, which may represent a possible mechanism linking AnglI and ATIR with angiogenesis. Additionally, AngⅡ-induced NO synthesis through eNOS in EPCs regulates apoptosis and adhesion, and the PI3-kinase/Akt pathway has an essential role in AngⅡ-induced antiapoptosis signaling.
