Regression of atherosclerosis in apolipoprotein E-deficient mice by lentivirus-mediated gene silencing of lipoprotein-associated phospholipase A2

2012 ◽  
Vol 427 (3) ◽  
pp. 557-562 ◽  
Author(s):  
Hui Zhang ◽  
Jinying Zhang ◽  
Deliang Shen ◽  
Li Zhang ◽  
Fei He ◽  
...  
Keyword(s):  
Gene Silencing ◽  
Phospholipase A2 ◽  
Apolipoprotein E ◽  
Deficient Mice

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 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

Prevention of Fatty Streak Formation of 17β-Estradiol Is Not Mediated by the Production of Nitric Oxide in Apolipoprotein E– Deficient Mice

Circulation ◽  
1997 ◽  
Vol 96 (9) ◽  
pp. 3048-3052 ◽  
Author(s):  
R. Elhage ◽  
F. Bayard ◽  
V. Richard ◽  
P. Holvoet ◽  
N. Duverger ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Apolipoprotein E ◽  
Fatty Streak ◽  
17Β Estradiol ◽  
Deficient Mice
Sign in / Sign up

Export Citation Format

Share Document