Apoptotic bodies from endothelial cells enhance the number and initiate the differentiation of human endothelial progenitor cells in vitro
Apoptotic bodies from endothelial cells enhance the number and initiate the differentiation of human endothelial progenitor cells in vitro
复制标题
DOI：
10.1182/blood-2003-10-3614
复制
发表时间：
2004-11-01
期刊：
影响因子：
20.3
通讯作者：
Weber, PC
中科院分区：
文献类型：
--
作者：
Hristov, M;Erl, W;Weber, PC
内皮祖细胞在缺血或损伤组织的修复中起着重要作用。由于内皮损伤可能与细胞凋亡相关，我们研究了成熟内皮细胞(ECs)的凋亡体是否会在体外影响内皮祖细胞的生长和分化。分离的人内皮祖细胞与来自内皮细胞的富含凋亡小体的培养液(ABRM)孵育24小时后，梭形附着细胞的数量显著增加。Dil-ac-低密度脂蛋白/凝集素染色、CD34和KDR表达检测鉴定内皮祖细胞。ABRM治疗后，Dil-ac-LDL/Lectin阳性细胞数增加2倍，CD34表达上调(22%+/-2%比13%+/-3%，P<0.05)，KDR表达上调(49%+/-12%比19%+/-7%，P<；0.05)。荧光和激光共聚焦显微镜显示内皮祖细胞摄取了凋亡小体。去凋亡体的培养液没有作用，而与凋亡体悬液孵育所产生的效应与ABRM相似。我们的结果表明，内皮细胞中的凋亡体被内皮祖细胞摄取，增加了它们的数量和分化状态。这种机制可能促进受损内皮细胞的修复，并可能是祖细胞和受损体细胞之间的一条新的信号通路。(C)2004年，由美国血液病学会提供。
Endothelial progenitor cells (EPCs) play a role in the repair of ischemic or injured tissue. Because endothelial injury can be associated with apoptosis, we have investigated whether apoptotic bodies from mature endothelial cells (ECs) may affect growth and differentiation of EPCs in vitro. A 24-hour incubation of isolated human EPCs with apoptotic bodies-rich medium (ABRM) from ECs led to a significant increase in the number of spindle-shaped attached cells. EPCs were characterized by Dil-Ac-LDL/lectin staining and measurement of CD34 and kinase insert domain receptor (KDR) expression. The treatment with ABRM resulted in a 2-fold increase of Dil-Ac-LDL/lectin-positive cells and up-regulation of CD34 (22% +/- 2% versus 13% +/- 3%, P < .05 and KDR (49% +/- 12% versus 19% +/- 7%, P < .05). Fluorescence and confocal laser microscopy demonstrated the uptake of apoptotic bodies by the EPCs. Apoptotic bodies-depleted medium had no effect, whereas the incubation with suspension of apoptotic bodies induced effects similar to those of ABRM. Our results suggest that apoptotic bodies from ECs are taken up by EPCs, increasing their number and differentiation state. Such a mechanism may facilitate the repair of injured endothelium and may represent a new signaling pathway between progenitor and damaged somatic cells. (C) 2004 by The American Society of Hematology.