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运动训练对有或无心肌梗死的小鼠内皮祖细胞功能诱导产生不同的改善情况。

Exercise training-induced different improvement profile of endothelial progenitor cells function in mice with or without myocardial infarction.

作者信息

Guo Yuan, Peng Ran, Liu Qiong, Xu Danyan

机构信息

Department of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, PR China.

Department of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, PR China.

出版信息

Int J Cardiol. 2016 Oct 15;221:335-41. doi: 10.1016/j.ijcard.2016.07.070. Epub 2016 Jul 5.

DOI:10.1016/j.ijcard.2016.07.070
PMID:27404702
Abstract

BACKGROUND

Neovascularization in response to ischemia after myocardial infarction (MI) has been widely considered as being initiated by endothelial progenitor cells (EPCs). Well-documented evidences in recent years have proved exercise training (ET) improving EPC function. However, whether ET-induced improvement of EPC function under or without ischemic state is different has not been reported.

METHODS

Mice performed ET following an exercise prescription 1week after MI or non-MI surgery respectively. Bone marrow-derived EPCs were isolated at 0day, 3days, 1week, 2weeks, 4weeks, and 8weeks of ET. After 7days cultivation, EPC functions including proliferation, adhesion, migration, and in vitro angiogenesis were measured. AKT/glycogen synthase kinase 3β (GSK3β) signaling pathway was tested by western blotting.

RESULTS

EPC function in mice underwent non-MI surgery was attenuated overtime, while ET ameliorated this tendency. EPC function was peaked at 4weeks ET in non-MI surgery mice and maintained with an extended exercise time. Besides, simple ischemia was sufficient to enhanced EPC function, with a maximum at 2weeks of MI surgery. In MI mice, ET further improved EPC function and achieved peak at 2weeks exercise. Furthermore, AKT/GSK3β signaling pathway activation was consistent with EPC function change after ischemia, which was further promoted by 4weeks exercise.

CONCLUSION

ET significantly increased EPC function in mice both with and without MI, but the time points of peak function were different.

摘要

背景

心肌梗死(MI)后缺血引起的新生血管形成一直被广泛认为是由内皮祖细胞(EPCs)启动的。近年来有充分证据证明运动训练(ET)可改善EPC功能。然而,ET在缺血或非缺血状态下对EPC功能改善的差异尚未见报道。

方法

分别在MI或非MI手术后1周,按照运动处方对小鼠进行ET。在ET的0天、3天、1周、2周、4周和8周分离骨髓来源的EPCs。培养7天后,检测EPC的增殖、黏附、迁移和体外血管生成等功能。通过蛋白质印迹法检测AKT/糖原合酶激酶3β(GSK3β)信号通路。

结果

非MI手术小鼠的EPC功能随时间衰减,而ET改善了这种趋势。在非MI手术小鼠中,EPC功能在ET 4周时达到峰值,并随运动时间延长而维持。此外,单纯缺血足以增强EPC功能,在MI手术后2周达到最大值。在MI小鼠中,ET进一步改善EPC功能,并在运动2周时达到峰值。此外,AKT/GSK3β信号通路的激活与缺血后EPC功能变化一致,运动4周进一步促进了这种变化。

结论

ET显著增加了MI和非MI小鼠的EPC功能,但功能峰值的时间点不同。

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