scholarly journals Amelioration of atherosclerosis in apolipoprotein E-deficient mice by combined RNA interference of lipoprotein-associated phospholipase A2 and YKL-40

PLoS ONE ◽  
2018 ◽  
Vol 13 (8) ◽  
pp. e0202797 ◽  
Author(s):  
Hui Zhang ◽  
Wenping Zhou ◽  
Chang Cao ◽  
Wenjing Zhang ◽  
Gangqiong Liu ◽  
...  
Keyword(s):  
Rna Interference ◽  
Phospholipase A2 ◽  
Apolipoprotein E ◽  
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 Amelioration of atherosclerosis in apolipoprotein E-deficient mice by inhibition of lipoprotein-associated phospholipase A2

2013 ◽  
Vol 36 (1) ◽  
pp. 32 ◽  
Author(s):  
Hui Zhang ◽  
Jin-Ying Zhang ◽  
Tong-Wen Sun ◽  
De-Liang Shen ◽  
Fei He ◽  
...  
Keyword(s):  
Phospholipase A2 ◽  
Apolipoprotein E ◽  
Inflammatory Cytokines ◽  
Negative Control ◽  
Therapeutic Effects ◽  
Inflammatory Gene Expression ◽  
Plaque Area ◽  
Atherosclerotic Lesions ◽  
Deficient Mice ◽  
Pro Inflammatory Cytokines

Purpose: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is involved in the pathogenesis of atherosclerosis, especially in advanced plaques. In the present study, the abilities of darapladib, a selective Lp-PLA2 inhibitor, and lentivirus-mediated Lp-PLA2 silencing on inflammation and atherosclerosis in apolipoprotein E-deficient mice were compared. Methods: Apolipoprotein E-deficient mice were fed on a high-fat diet and a constrictive collar was placed around the left carotid artery to induce plaque formation. The mice were randomly divided into control, negative control (NC), darapladib and RNA interference (RNAi) groups. Eight weeks after surgery, lentivirus-mediated RNAi construct or darapladib were used to decrease the expression of Lp-PLA2. Plaques were collected five weeks later for histological analysis. Inflammatory gene expression in the atherosclerotic lesions were then determined at the mRNA and protein level. Results: The expression of pro-inflammatory cytokines was significantly reduced in the treatment group, compared to nontreatment group, whereas the plasma concentration of anti-inflammatory cytokines increased markedly. Moreover, our results demonstrated a significant reduction in plaque lipid content, as well as a rise in collagen content following Lp-PLA2 inhibition. Interestingly, when comparing the two methods of Lp-PLA2 inhibition, animals treated with Lp-PLA2 RNAi were found to exhibit lower plaque areas and enhanced improvement of plaque stability as compared with animals treated with darapladib. Darapladib had no attenuating effect on atherosclerotic plaque area. These therapeutic effects were independent of plasma lipoprotein levels. Conclusions: Lp-PLA2 inhibition by darapladib or lentivirus-mediated RNAi ameliorated inflammation and atherosclerosis in apolipoprotein E-deficient mice. The effect was more prominent in the RNAi group.

Phospholipase A2 activity is decreased selectively in the hippocampus of aged apolipoprotein E deficient mice

2000 ◽  
Vol 288 (3) ◽  
pp. 211-214 ◽  
Author(s):  
Casey B Patrick ◽  
Pascale Krzywkowski ◽  
Charles Ramassamy ◽  
Judes Poirier ◽  
Stanley I Rapoport ◽  
...  
Keyword(s):  
Phospholipase A2 ◽  
Apolipoprotein E ◽  
Phospholipase A2 Activity ◽  
Deficient Mice

scholarly journals RNA Interference of Myocyte Enhancer Factor 2A Accelerates Atherosclerosis in Apolipoprotein E-Deficient Mice

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0121823 ◽  
Author(s):  
Wen-ping Zhou ◽  
Hui Zhang ◽  
Yu-xia Zhao ◽  
Gang-qiong Liu ◽  
Jin-ying Zhang
Keyword(s):  
Rna Interference ◽  
Apolipoprotein E ◽  
Myocyte Enhancer Factor ◽  
Deficient Mice ◽  
Enhancer Factor
Sign in / Sign up

Export Citation Format

Share Document