DJ-1 Alleviates Angiotensin II-Induced Endothelial Progenitor Cell Damage by Activating the PPAR/HO-1 Pathway

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.