DJ-1 Alleviates Angiotensin II-Induced Endothelial Progenitor Cell Damage by Activating the PPAR/HO-1 Pathway
DJ-1 Alleviates Angiotensin II-Induced Endothelial Progenitor Cell Damage by Activating the PPAR/HO-1 Pathway
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DOI：
10.1002/jcb.26191
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发表时间：
2018-01-01
影响因子：
4
通讯作者：
Yang, Songbai
中科院分区：
文献类型：
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作者：
Han, Tao;Liu, Meihan;Yang, Songbai
有证据表明血管紧张素II(Ang II)可能损害内皮祖细胞(EPC)的功能。结果表明，DJ-1具有抗氧化应激作用。在本研究中，我们研究了DJ-1是否对血管紧张素Ⅱ诱导的细胞损伤具有保护作用。Ang II组内皮祖细胞的增殖和迁移明显减少，而DJ-1的过度表达则促进了EPC的增殖和迁移。Western blotting结果显示，Ang II诱导的衰老标志物半乳糖苷酶表达增加和黏附分子(ICAM-1、VCAM-1)表达降低在Ad-DJ-1转染后发生逆转。经Ad-DJ-1基因转染后，血管紧张素Ⅱ诱导的内皮细胞血管生成能力下降的情况也得到改善。Ang II可显著升高心肌细胞内ROS、丙二醛(MDA)、炎性细胞因子(TNF-、IL-1)水平，降低超氧化物歧化酶(SOD)、谷胱甘肽(GSH)水平，而Ad-DJ-1可逆转上述作用。DJ-1可增加PPAR和HO-1的表达。因此，构建了HO-1 siRNA，并将其导入内皮祖细胞，结果显示HO-1 siRNA可抑制DJ-1对EPC功能的影响。因此，我们的研究表明，DJ-1可能通过激活PPAR/HO-1来保护EPC免受Ang II诱导的功能障碍。J.细胞。生物化学。2018年，119：392-400。(C)2017威利期刊公司。
There is evidence that angiotensin II (Ang II) may impair the functions of endothelial progenitor cells (EPCs). It was revealed that DJ-1 could resist oxidative stress. In this study, we investigated whether DJ-1 could protect EPCs against Ang II-induced cell damage. The proliferation and migration of EPCs were strongly reduced in the Ang II group and were increased by overexpression of DJ-1. Western blotting indicated that the increased expression of the senescence marker -galactosidase and decreased expression of adhesion molecules (ICAM-1, VCAM-1) induced by Ang II were reversed after Ad-DJ-1 transfection. The reduced angiogenic capacity of EPCs caused by Ang II was also improved after Ad-DJ-1 transfection. Moreover, Ang II significantly increased the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and inflammatory cytokines (TNF- and IL-1), reduced the levels of superoxide dismutase (SOD), glutathione (GSH), and these were reversed by Ad-DJ-1 transfection. Expression of peroxisome proliferator-activated receptor- (PPAR) and heme oxygenase (HO-1) was increased by DJ-1. Therefore, HO-1 siRNA were constructed and transfected into EPCs, and the results showed that HO-1 siRNA transfection inhibited the effects of DJ-1 on EPC function. Thus, our study implies that DJ-1 may protect EPCs against Ang II-induced dysfunction by activating the PPAR/HO-1. J. Cell. Biochem. 119: 392-400, 2018. (c) 2017 Wiley Periodicals, Inc.