Research Papers: Gerotarget (Focus on Aging):
VPO1 mediates oxidation of LDL and formation of foam cells
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Youfeng Yang1,*, Ruizheng Shi1,2,*, Zehong Cao1, Guogang Zhang2 and Guangjie Cheng1
1 Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA
2 Department of Cardiovascular Medicine, Xiangya Hospital, Central South University, Changsha, China
* These authors have contributed equally to this work
Guangjie Cheng, email:
Keywords: heme-containing peroxidase; free radical; low-density lipoprotein; oxidized lipids; foam cells; Gerotarget
Received: March 09, 2016 Accepted: April 24, 2016 Published: May 05, 2016
Deposition of oxidized-LDL in vascular walls is essential in the initiation of atherosclerosis. Oxidation of LDL has been attributed to myeloperoxidase as its generation of potent oxidants. However, the exact mechanism of LDL oxidation and foam cell formation in atherosclerosis remains to be elucidated. Vascular peroxidase-1 (VPO1), a newly-identified heme-containing peroxidase, is primarily expressed in cardiovascular systems, and secreted into the circulation. The present study evaluates VPO1-mediated LDL oxidation and its role in atherosclerosis. VPO1 was first demonstrated binding to LDL. VPO1-mediated oxidation of proteins and lipids in LDL was verified by a variety of methods including immunoblot analysis, free tryptophan assay, UV absorbance, and thiobarbituric acid assay. VPO1-oxidized LDL caused accumulation of LDL in monocyte-like cells and promoted formation of foam cells. Administration of inflammation factors, LPS or TNF-α, induced increasing expression of VPO1 in aorta and secretion to plasma. TNF-α also promoted formation and retention of VPO1-oxidized LDL in aortic walls. Our data suggest that VPO1 contributes to oxidation and retention of LDL in vessel walls, and formation foam cells, indicating VPO1 as a novel potential mediator of atherosclerosis.
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