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内皮祖细胞分泌SDF1及其抗内皮祖细胞凋亡作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2007年第4期
页码:
391-394
栏目:
基础研究
出版日期:
2007-08-01

文章信息/Info

Title:
Endothelial progenitor cells secrete SDF1 and SDF1 protects endothelial progenitor cells from apoptosis
作者:
尹扬光1; 黄岚1 ; 赵晓辉1; 于世勇1; 方玉强2; 赵景红1
第三军医大学：1.新桥医院心内科，重庆400037, 2.大坪医院心内科
Author(s):
YIN Yangguang;  HUANG Lan;  ZHAO Xiaohui;  YU Shiyong;  FANG Yuqiang;  ZHAO Jinghong
Department of Cardiology, Xin Qiao Hospital, Third Military Medical University, Chongqing 400037, China
关键词:
基质细胞衍生因子1; AMD3100; 内皮祖细胞; 凋亡
Keywords:
stromal cellderived factor1;  AMD3100;  endothelial progenitor cells;  apoptosis
分类号:
R329.2
DOI:
-
文献标识码:
A
摘要:
目的 探讨内皮祖细胞（EPC）能否分泌基质细胞衍生因子1（SDF1），及SDF1能否抑制紫杉醇、AMD3100（特异性阻断SDF1与其受体CXCR4结合）等诱导的EPC凋亡。方法 取不同时间段的EPC培养液上清，采用ELISA检测上清中SDF1a浓度。用不同浓度的紫杉醇、AMD3100及无血清培养诱导EPC凋亡；或在上述基础上加不同浓度的SDF1a处理；48 h后采用TUNEL法和流式细胞仪检测各组EPC凋亡率。结果 EPC培养液上清中SDF1a浓度显著高于对照组（P<0.01）。紫杉醇、AMD3100和无血清培养一样，均可显著增高EPC凋亡率（P<0.01）；加入外源性SDF1a可显著降低紫杉醇组、无血清培养组EPC凋亡率（P<0.01），却不能降低AMD3100组EPC凋亡率。结论 体外培养的EPC可分泌SDF1a，采用AMD3100阻断其作用可诱导EPC凋亡；SDF1a可对抗紫杉醇和无血清培养诱导的EPC凋亡，但对AMD3100诱导的凋亡无效。
Abstract:
AIM To investigate whether endothelial progenitor cells (EPC) can secrete stromal cellderived factor1（SDF1）and whether SDF1 can inhibit paclitaxel, AMD3100 and serum starvationinduced apoptosis in EPC. METHODS SDF1 in cell culture supernates was determined by enzymelinked immunosorbent assay. To induce apoptosis, EPC in 96 or 24well plates were replaced with media containing different concentrations of paclitaxel, AMD3100（an antagonist of CXCR4）or serum absent media and were incubated for 48 h. Or under the above conditions, the medium was supplemented with different concentrations of SDF1. After 48 h incubation, apoptosis was determined by TUNEL method and flow cytometry. RESULTS SDF1 concentration in cell culture supernates was higher than that in endothelial basal medium（P<0.01）. Paclitaxel, AMD3100 and serum starvation all increased apoptosis in both EPC and control（P<0.01）. SDF1 reduced apoptosis induced by paclitaxel or serum starvation in EPC (P<0.01), but not reduce AMD3100induced EPC apoptosis. CONCLUSION In vitro, EPC secretes SDF1 and blocking its effect by AMD3100 induces EPC apoptosis. SDF1 protects EPC from paclitaxel or serum starvationinduced apoptosis, but not from AMD3100induced apoptosis.

参考文献/References

［1］Jia L, Takahashi M, Yoshioka T, et al. Therapeutic potential of endothelial progenitor cells for cardiovascular diseases［J］. Curr Vasc Pharmacol，2006，4(1):5965.

［2］Askari AT, Unzek S, Popovic ZB, et al. Effect of stromal cellderived factor1 on stem cell homing and tissue regeneration in ischemic cardiomyopathy［J］. Lancet，2003，362 (9385):697-703.

［3］Lataillade JJ, Clay D, Dupuy C, et al. Chemokine SDF1 enhances circulating CD34(+) cell proliferation in synergy with cytokines: possible role in progenitor survival［J］. Blood，2000，95(3):756-68.

［4］Werner N, Junk S, Laufs U, et al. Intravenous transfusion of endothelial progenitor cells reduces neointima formation after vascular injury［J］. Circ Res，2003，93(2):e17-e24.

［5］Loetscher M, Geiser T , O′Reilly T , et al . Cloning of a human seven transmembrane domain receptor , LESTR , that is highly expressed in leukocytes［J］. J Biol Chem，1994，269 (1):232 - 237.

［6］Yamaguchi J, Kusano KF, Masuo O, et al. Stromal cellderived factor1 effects on ex vivo expanded endothelial progenitor cells recruitment for ischemic neovascularization［J］. Circulation，2003，107(9):13221328.

［7］Lataillade JJ, Domenech J, Le BousseKerdiles MC. Stromal cellderived factor1 (SDF1)CXCR4 couple plays multiple roles on haematopoietic progenitors at the border between the old cytokine and new chemokine worlds: survival, cell cycling and trafficking［J］. Eur Cytokine Netw，2004，15(3):177-188.

［8］De Falco E, Porcelli D, Torella AR, et al. SDF1 involvement in endothelial phenotype and ischemiainduced recruitment of bone marrow progenitor cells［J］. Blood，2004，104(12):3472-3482.

［9］Zernecke A, Schober A, Bot I, et al. SDF1alpha/CXCR4 axis is instrumental in neointimal hyperplasia and recruitment of smooth muscle progenitor cells［J］. Circ Res,2005,96（7）:784-791.

备注/Memo

备注/Memo:
收稿日期：2006-06-23.通讯作者：黄岚，教授，主要从事冠心病防治、血管损伤与修复研究Email：huanglans@21cn.com 作者简介：尹扬光，主治医师，博士生 Email:yyg751203@soho.com
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