VNN1 promotes atherosclerosis progression in apoE−/− mice fed a high-fat/high-cholesterol diet

• DOI: 10.1194/jlr.m065565
• Publication Date: 2016-06-09T19:47:37Z
• Authors: Yan-Wei Hu; Shao-Guo Wu; Jing-Jing Zhao; Xin Ma; Jing-Bo Lu; Jian-cheng Xiu; Yuan Zhang; Chuan Huang; Yu-Rong Qiu; Yan-Hua Sha; Ji-Juan Gao; Yan-Chao Wang; Shu-Fen Li; Jia-Yi Zhao; Lei Zheng; Qian Wang
• Keywords: Apolipoprotein E; Foam cell

Accumulated evidence shows that vanin-1 (VNN1) plays a key part in glucose metabolism. We explored the effect of VNN1 on cholesterol metabolism, inflammation, apoptosis vitro, and progression atherosclerotic plaques apoE^−/− mice. Oxidized LDL (Ox-LDL) significantly induced expression through an ERK1/2/cyclooxygenase-2/PPARα signaling pathway. increased cellular content decreased apoAI HDL-cholesterol (HDL-C)-mediated efflux by 25.16% 23.13%, respectively, THP-1 macrophage-derived foam cells (<i>P</i> < 0.05). In addition, attenuated Ox-LDL-induced upregulation p53 59.15% downregulation B-cell lymphoma-2 127.13% macrophage vivo, mice were divided randomly into two groups transduced with lentivirus (LV)-Mock or LV-VNN1 for 12 weeks. VNN1-treated showed liver lipid plasma levels TG (124.48%), LDL-cholesterol (119.64%), TNF-α (148.74%), interleukin (IL)-1β (131.81%), IL-6 (156.51%), whereas HDL-C (25.75%) Consistent these data, development lesions was upon infection LV-VNN1. These observations suggest may be promising therapeutic candidate against atherosclerosis.