Dihydrotanshinone I Attenuates Plaque Vulnerability in Apolipoprotein E-Deficient Mice: Role of Receptor-Interacting Protein 3

2020 ◽  
Author(s):  
Wenwen Zhao ◽  
Chunxia Li ◽  
Hao Zhang ◽  
Qihui Zhou ◽  
Xuehong Chen ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Plaque Vulnerability ◽  
Interacting Protein ◽  
Deficient Mice

scholarly journals Chronic iron overload intensifies atherosclerosis in apolipoprotein E deficient mice: Role of oxidative stress and endothelial dysfunction

Life Sciences ◽  
2019 ◽  
Vol 233 ◽  
pp. 116702 ◽  
Author(s):  
Vinícius Bermond Marques ◽  
Marcos André Soares Leal ◽  
Jandinay Gonzaga Alexandre Mageski ◽  
Helbert Gabriel Fidelis ◽  
Breno Valentim Nogueira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Iron Overload ◽  
Apolipoprotein E ◽  
Deficient Mice

scholarly journals Role of Interleukin 17A in Aortic Valve Inflammation in Apolipoprotein E-deficient Mice

2020 ◽  
Vol 40 (4) ◽  
pp. 729-738
Author(s):  
Fa-yuan Liu ◽  
Peng Bai ◽  
Ye-fan Jiang ◽  
Nian-guo Dong ◽  
Geng Li ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Apolipoprotein E ◽  
Interleukin 17A ◽  
Deficient Mice

scholarly journals Role of Toll-Like Receptor 4 in Intimal Foam Cell Accumulation in Apolipoprotein E–Deficient Mice

2011 ◽  
Vol 31 (1) ◽  
pp. 50-57 ◽  
Author(s):  
Mie Higashimori ◽  
Jeffrey B. Tatro ◽  
Kathryn J. Moore ◽  
Michael E. Mendelsohn ◽  
Jonas B. Galper ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Foam Cell ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Cell Accumulation ◽  
Deficient Mice

scholarly journals Critical Role of Macrophage 12/15-Lipoxygenase for Atherosclerosis in Apolipoprotein E–Deficient Mice

Circulation ◽  
2004 ◽  
Vol 110 (14) ◽  
pp. 2024-2031 ◽  
Author(s):  
Yuqing Huo ◽  
Lei Zhao ◽  
Matthew Craig Hyman ◽  
Pavel Shashkin ◽  
Brian L. Harry ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Critical Role ◽  
Deficient Mice

scholarly journals Silence of NLRP3 Suppresses Atherosclerosis and Stabilizes Plaques in Apolipoprotein E-Deficient Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Fei Zheng ◽  
Shanshan Xing ◽  
Zushun Gong ◽  
Wei Mu ◽  
Qichong Xing
Keyword(s):  
Rna Interference ◽  
Apolipoprotein E ◽  
Nlrp3 Inflammasome ◽  
Vital Role ◽  
Nlrp3 Gene ◽  
New Strategy ◽  
Nlrp3 Inflammasomes ◽  
The Impact ◽  
Deficient Mice

Objectives. The role of the NLRP3 inflammasome in atherosclerosis remains controversial. The aim of this study was to determine whether inhibition of NLRP3 signaling by lentivirus-mediated RNA interference could reduce atherosclerosis and stabilizes plaques. We also tried to explore the mechanisms of the impact of NLRP3 inflammasome on atherosclerosis.Methods. Apolipoprotein E-deficient mice aged 8 weeks were fed a high-fat diet and were injected with NLRP3 interfering or mock viral suspension after 4 weeks. Lentivirus transfer was repeated in 2 weeks. Four weeks after the first lentivirus injection, we evaluated the effects of NLRP3 gene silencing on plaque composition and stability and on cholesterol efflux and collagen metabolism, by histopathologic analyses and real-time PCR.Results. Gene silence of NLRP3 prevented plaques progression and inhibited inductions of proinflammatory cytokines. Moreover, this RNA interference reduced plaque content of macrophages and lipid, and increased plaque content of smooth muscle cells and collagen, leading to the stabilizing of atherosclerotic plaques.Conclusions. NLRP3 inflammasomes may play a vital role in atherosclerosis, and lentivirus-mediated NLRP3 silencing would be a new strategy to inhibit plaques progression and to reduce local inflammation.

scholarly journals Apolipoprotein E receptor 2 is involved in the thrombotic complications in a murine model of the antiphospholipid syndrome

Blood ◽  
2011 ◽  
Vol 117 (4) ◽  
pp. 1408-1414 ◽  
Author(s):  
Zurina Romay-Penabad ◽  
Renan Aguilar-Valenzuela ◽  
Rolf T. Urbanus ◽  
Ronald H. W. M. Derksen ◽  
Maarten T. T. Pennings ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Thrombus Formation ◽  
Convincing Evidence ◽  
Wild Type ◽  
Glycoprotein I ◽  
Thrombotic Complications ◽  
Deficient Mice ◽  
Pathogenic Effects

Abstract Antiphospholipid (aPL)/anti-β2 glycoprotein I (anti-β2GPI) antibodies stimulates tissue factor (TF) expression within vasculature and in blood cells, thereby leading to increased thrombosis. Several cellular receptors have been proposed to mediate these effects, but no convincing evidence for the involvement of a specific one has been provided. We investigated the role of Apolipoprotein E receptor 2 (ApoER2′) on the pathogenic effects of a patient-derived polyclonal aPL IgG preparation (IgG-APS), a murine anti-β2GPI monoclonal antibody (E7) and of a constructed dimeric β2GPI I (dimer), which in vitro mimics β2GPI-antibody immune complexes, using an animal model of thrombosis, and ApoER2-deficient (−/−) mice. In wild type mice, IgG-APS, E7 and the dimer increased thrombus formation, carotid artery TF activity as well as peritoneal macrophage TF activity/expression. Those pathogenic effects were significantly reduced in ApoER2 (−/−) mice. In addition, those effects induced by the IgG-APS, by E7 and by the dimer were inhibited by treatment of wild-type mice with soluble binding domain 1 of ApoER2 (sBD1). Altogether these data show that ApoER2 is involved in pathogenesis of antiphospholipids antibodies.

scholarly journals Role of Interleukin 17 in Inflammation, Atherosclerosis, and Vascular Function in Apolipoprotein E–Deficient Mice

2011 ◽  
Vol 31 (7) ◽  
pp. 1565-1572 ◽  
Author(s):  
Meena S. Madhur ◽  
Samuel A. Funt ◽  
Li Li ◽  
Antony Vinh ◽  
Wei Chen ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Vascular Function ◽  
Interleukin 17 ◽  
Deficient Mice
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