Enhanced Stabilization of Atherosclerotic Plaques in Apolipoprotein E-Knockout Mice by Combinatorial Toll-like Receptor-1 and -2 Gene Silencing

2009 ◽  
Vol 20 (7) ◽  
pp. 739-750 ◽  
Author(s):  
Li Hang Qi ◽  
Ying Wang ◽  
Fei Gao ◽  
Cheng Zhang ◽  
Shi Fang Ding ◽  
...  
Keyword(s):  
Gene Silencing ◽  
Apolipoprotein E ◽  
Knockout Mice ◽  
Atherosclerotic Plaques ◽  
Toll Like Receptor ◽  
Apolipoprotein E Knockout Mice

Hydrogen sulfide stabilizes atherosclerotic plaques in apolipoprotein E knockout mice

2019 ◽  
Vol 144 ◽  
pp. 90-98 ◽  
Author(s):  
Qinghui Xiong ◽  
Zhijun Wang ◽  
Ying Yu ◽  
Yadan Wen ◽  
Rinkiko Suguro ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Apolipoprotein E ◽  
Knockout Mice ◽  
Atherosclerotic Plaques ◽  
Apolipoprotein E Knockout Mice

scholarly journals Effects of Chronic Mild Stress on the Development of Atherosclerosis and Expression of Toll-Like Receptor 4 Signaling Pathway in Adolescent Apolipoprotein E Knockout Mice

2009 ◽  
Vol 2009 ◽  
pp. 1-13 ◽  
Author(s):  
Hongfeng Gu ◽  
Chaoke Tang ◽  
Kuang Peng ◽  
Hui Sun ◽  
Yongzong Yang
Keyword(s):  
Apolipoprotein E ◽  
Signaling Pathway ◽  
Knockout Mice ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Apolipoprotein E Knockout Mice ◽  
Tlr4 Signaling Pathway ◽  
Myeloid Differentiation Factor

Here, we investigated the effect of chronic mild stress (CMS) on the development of atherosclerosis as well as the expression of Toll-like receptors (TLRs) signaling pathway in adolescent apolipoprotein E knockout (apoE-/-) mice. Mice were subjected to daily CMS for 0, 4, and 12 weeks, respectively. To identify the expression of Toll-like receptor 4 signaling pathway in adolescent apolipoprotein E knockout mice subjected to CMS, we compared gene expression in aortas of stressed and unstressed mice using TLRs signaling pathway real-time PCR microarrays consisting of 87 genes. We found that atherosclerosis lesions both in aortic tress and sinuses of CMS mice were significantly increased linearly in response to duration of CMS exposure. Among 87 genes analyzed, 15 genes were upregulated in stressed mice, especially TLR4, myeloid differentiation factor 88 (MyD88), and IL-1β, and 28 genes were downregulated compared with nonstressed mice. CMS mice demonstrated markedly increased aortic atherosclerosis that were associated with significant increases in levels of expression of TLR4, MyD88, nuclear factorκB (NF-κB), MCP-1, IL-1β, TNF-α, and sICAM-1. Taken together, our results suggest an important role for TLR4 signaling pathway in atherosclerosis in a CMS mouse model.

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