Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5944124 | Atherosclerosis | 2015 | 13 Pages |
Abstract
Oxidised lipoprotein(a) [oxLp(a)] is considered as a more potent arteriosclerotic factor than native Lp(a). However, the molecular mechanisms underlying this potency remain unclear. Reactive oxygen species (ROS) possibly act as intracellular second messengers that participate in autophagy stimulation. In this study, the effect of oxLp(a) on endothelial cell autophagy was determined. The mechanism and effect of autophagy on endothelial cells were also investigated. Results showed that oxLp(a) could induce autophagy depending on the generation of cellular ROS. Superoxide dismutase, an antioxidant, could inhibit oxLp(a)-induced autophagy in human umbilical vascular endothelial cells. Furthermore, poly(adenosine diphosphate-ribose) polymerase-1 (PARP-1)-liver kinase B1 (LKB1)-adenosine monophosphate-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR) and LKB1-AMPK-mTOR pathways are involved in oxLp(a)-induced autophagy. These pathways are also dependent on ROS. Thus, oxLp(a) induced autophagy via LKB1-AMPK-mTOR and PAPR-1-LKB1-AMPK-mTOR pathways, which are dependent on ROS generation.
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Authors
Guo-hua Li, Xiao-long Lin, Hai Zhang, Shuang Li, Xing-lan He, Kai Zhang, Juan Peng, Ya-ling Tang, Jun-fa Zeng, Yue Zhao, Xiao-feng Ma, Jian-jun Lei, Ren Wang, Dang-heng Wei, Zhi-Sheng Jiang, Zuo Wang,