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脂多糖损害了内皮祖细胞的功能活性。

Lipopolysaccharide impaired the functional activity of endothelial colony-forming cells.

作者信息

Yu Min, Zhang Qingying, Liu Qian, Sun Jing, Yang Guibao, Zeng Guoning, Tan Xuerui

机构信息

Department of Cardiology, First Affiliated Hospital, Shantou University Medical College, Shantou, PR China.

出版信息

Respiration. 2014;87(4):317-23. doi: 10.1159/000357438. Epub 2014 Jan 21.

Abstract

BACKGROUND

Recent studies have shown that endothelial progenitor cells (EPCs) contribute to lung repair after lipopolysaccharide (LPS)-induced lung injury and infusion of LPS decreased early EPCs in human peripheral blood. However, the effects of LPS on endothelial colony-forming cells (ECFCs) remain to be determined.

OBJECTIVE

To investigate possible effects of LPS on the functional activity of ECFCs.

METHODS

ECFCs were isolated from human umbilical cord blood and characterized. ECFCs at passages 3-5 were treated for 24 h with either LPS or vehicle control. Their viability, migration and in vitro vasculogenesis activity were assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, modified Boyden chamber and in vitro angiogenesis assays, respectively. ECFC adhesion was assessed by replating cells on fibronectin-coated dishes and subsequent counting of adherent cells.

RESULTS

Incubation with LPS dose-dependently inhibited the viable, migratory, adhesive and in vitro vasculogenesis capacity of ECFCs.

CONCLUSION

LPS impaired the functional activity of ECFCs.

摘要

背景

近期研究表明,内皮祖细胞(EPCs)有助于脂多糖(LPS)诱导的肺损伤后的肺修复,且输注LPS会降低人外周血中早期EPCs的数量。然而,LPS对内皮集落形成细胞(ECFCs)的影响仍有待确定。

目的

研究LPS对ECFCs功能活性的可能影响。

方法

从人脐带血中分离并鉴定ECFCs。对第3 - 5代的ECFCs用LPS或溶剂对照处理24小时。分别通过3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐、改良的Boyden小室和体外血管生成试验检测其活力、迁移和体外血管生成活性。通过将细胞重新接种到纤连蛋白包被的培养皿上并随后计数贴壁细胞来评估ECFC的黏附情况。

结果

与LPS孵育剂量依赖性地抑制了ECFCs的活力、迁移、黏附及体外血管生成能力。

结论

LPS损害了ECFCs的功能活性。

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