Journal
FEBS LETTERS
Volume 588, Issue 23, Pages 4448-4456Publisher
WILEY
DOI: 10.1016/j.febslet.2014.09.046
Keywords
Endothelial cell; Hypoxia; Very low density lipoprotein receptor; Endoplasmic reticulum stress; Apoptosis
Funding
- Natural Science Foundation of Shanghai Municipal Science and Technology Commission [14ZR1437400]
- Shanghai Municipal Science and Technology Commission grant [124119b1800]
- Shanghai Municipal Commission of Health and Family Planning grant [20124443]
- Key Disciplines Group Construction Project of Pudong Health Bureau of Shanghai [PWZxq2014-08]
- Discipline Leader Project of Pudong Health Bureau of Shanghai [PWRd2013-08]
- Outstanding Youth Medical Talents of Pudong Health Bureau of Shanghai [PWRq2013-10]
- Pujiang Talent Program of Shanghai Municipal Science and Technology Commission
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Endothelial cells express very low density lipoprotein receptor (VLDLr). Beyond the function as peripheral lipoprotein receptor, other roles of VLDLr in endothelial cells have not been completely unraveled. In the present study, human umbilical vein endothelial cells were subjected to hypoxia, and VLDLr expression, endoplasmic reticulum (ER) stress, and apoptosis were assessed. Hypoxia triggered endothelial ER stress and apoptosis, and induced VLDLr expression. Silencing or stabilization of HIF-1 alpha reduced and enhanced VLDLr expression, respectively. HIF-1 alpha affected vldlr promoter activity by interacting with a hypoxia-responsive element (HRE). Knockdown or overexpression of VLDLr alleviated and exacerbated hypoxia-induced ER stress and apoptosis, respectively. Thus, hypoxia induces VLDLr expression through the interaction of HIF-1 alpha with HRE at the vldlr promoter. VLDLr then mediates ER stress and apoptosis. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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