Inhibition of endoplasmic reticulum stress and oxidative stress by vitamin D in endothelial cells
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- 作者：Michael J. Haas ; michael.haas@jax.ufl.edu" class="auth_mail" title="E-mail the corresponding author ; Mohammad Jafri ; Kent R. Wehmeier ; Luisa M. Onstead-Haas ; Arshag D. Mooradian
- 关键词：CSPD ; 3-(diethylamino)-1-(2 ; 2-dimethyl-3-H-1-benzofuran-7-yl)-propan-1-one ; eIF2α ; eukaryotic initiation factor 2α ; DMSO ; dimethylsulfoxide ; EB ; EB1089 ; ER ; endoplasmic reticulum ; ES-TRAP ; placental secreted alkaline phosphatase ; GAPDH ; glyceraldehyde-3-phosphate dehydrogenase ; GRP 78 ; glucose-regulated protein 78 ; HBSS ; Hank's balanced salt solution ; HDL ; high-density lipoprotein ; HUVEC ; human umbilical vein endothelial cell ; ICAM 1 ; intercellular adhesion molecule 1 ; JNK1 ; c-jun N-terminal kin
- 刊名：Free Radical Biology and Medicine
- 出版年：2016
- 出版时间：October 2016
- 年：2016
- 卷：99
- 期：Complete
- 页码：1-10
- 全文大小：1558 K
文摘
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Vitamin D and its metabolites/analogs inhibited ER stress in endothelial cells.
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Similar effects were observed with hyperglycemia-induced ER stress and SO generation.
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Vitamin D prevented high-dextrose cell death.
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This suggests that vitamin D has a protective effect on endothelial cells.