1.P.79 The effect of lacidipine on atherosclerotic lesion progression in apoE knockout mice

1997 ◽  
Vol 134 (1-2) ◽  
pp. 33 ◽  
Author(s):  
P. Cristofori ◽  
A. Lanzoni ◽  
D. Spagnolo ◽  
L. Cominacini ◽  
A. Pastorino ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Atherosclerotic Lesion ◽  
Apoe Knockout Mice

HDL is essential for atherosclerotic lesion regression in Apoe knockout mice by bone marrow Apoe reconstitution

2018 ◽  
Vol 278 ◽  
pp. 240-249 ◽  
Author(s):  
Ronald J. van der Sluis ◽  
Robin A.F. Verwilligen ◽  
Zsuzsanna Lendvai ◽  
Robbert Wever ◽  
Menno Hoekstra ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Knockout Mice ◽  
Atherosclerotic Lesion ◽  
Apoe Knockout Mice ◽  
Lesion Regression

Postnatal inflammation following intrauterine inflammation exacerbates the development of atherosclerosis in ApoE−/− mice

2019 ◽  
Vol 133 (10) ◽  
pp. 1185-1196 ◽  
Author(s):  
Siroon Bekkering ◽  
Albert P. Limawan ◽  
Maria U. Nguyen ◽  
Lisa K. Widiasmoko ◽  
Hui Lu ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Early Life ◽  
Atherosclerotic Lesion ◽  
Lesion Size ◽  
Chronic Inflammatory Disease ◽  
Mechanistic Studies ◽  
Human Infants ◽  
Size Number ◽  
Severe Atherosclerosis ◽  
Apoe Knockout Mice

Abstract Atherosclerosis is a chronic inflammatory disease that has its origins in early life. Postnatal inflammation exacerbates atherosclerosis, but the possible effect of intrauterine inflammation is largely unexplored. Exposure to inflammation in utero is common, especially in infants born preterm, who have increased cardiovascular risk in adulthood. We hypothesised that exposure to inflammation before birth would accelerate the development of atherosclerosis, with the most severe atherosclerosis following exposure to both pre- and postnatal inflammation. Here we studied the effect of prenatal and postnatal inflammation on the development of atherosclerosis by combining established techniques for modelling histological chorioamnionitis and atherosclerosis using apolipoprotein E (ApoE) knockout mice. A single intra-amniotic (IA) injection of lipopolysaccharide (LPS) caused intrauterine inflammation, and increased atherosclerosis at 13 weeks of postnatal age. In mice exposed to postnatal LPS, chorioamnionitis modulated subsequent responses; atherosclerotic lesion size, number and severity were greatest for mice exposed to both intrauterine and postnatal inflammation, with a concomitant decrease in collagen content and increased inflammation of the atherosclerotic plaque. In conclusion, pre- and postnatal inflammation have additive and deleterious effects on the development of atherosclerosis in ApoE knockout mice. The findings are particularly relevant to preterm human infants, whose gestations are frequently complicated by chorioamnionitis and who are particularly susceptible to repeated postnatal infections. Human and mechanistic studies are warranted to guide preventative strategies.

scholarly journals Low-Cholesterol and High-Fat Diets Reduce Atherosclerotic Lesion Development in ApoE-Knockout Mice

1999 ◽  
Vol 19 (10) ◽  
pp. 2368-2375 ◽  
Author(s):  
Lucía Calleja ◽  
Miguel A. París ◽  
Antoni Paul ◽  
Elisabet Vilella ◽  
Jorge Joven ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Atherosclerotic Lesion ◽  
High Fat ◽  
Lesion Development ◽  
High Fat Diets ◽  
Apoe Knockout Mice ◽  
Fat Diets ◽  
Low Cholesterol ◽  
Atherosclerotic Lesion Development

PO9-223 TNF-LIKE INDUCER OF APOPTOSIS (TWEAK) INCREASES ATHEROSCLEROTIC LESION SIZE AND INFLAMMATION IN APOE KNOCKOUT MICE

2007 ◽  
Vol 8 (1) ◽  
pp. 72
Author(s):  
B. Muñoz-García ◽  
O. Lopez-Franco ◽  
J.L. Martín-Ventura ◽  
J.A. Moreno ◽  
J. Egido ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Atherosclerotic Lesion ◽  
Lesion Size ◽  
Apoe Knockout Mice

MS152 DEFICIENCY OF NPP1 ATTENUATES ATHEROSCLEROTIC LESION PROGRESSION IN apoE KNOCKOUT MICE

2010 ◽  
Vol 11 (2) ◽  
pp. 140
Author(s):  
Y. Nitschke ◽  
G. Weissen-Plenz ◽  
R. Terkeltaub ◽  
F. Rutsch
Keyword(s):  
Knockout Mice ◽  
Atherosclerotic Lesion ◽  
Apoe Knockout Mice

scholarly journals Overexpression of NF-κB p65 in macrophages ameliorates atherosclerosis in apoE-knockout mice

2013 ◽  
Vol 305 (11) ◽  
pp. E1375-E1383 ◽  
Author(s):  
Xin Ye ◽  
Xiaoting Jiang ◽  
Wei Guo ◽  
Katie Clark ◽  
Zhanguo Gao
Keyword(s):  
Fatty Acid ◽  
Energy Expenditure ◽  
Knockout Mice ◽  
Foam Cell ◽  
Cell Formation ◽  
Atherosclerotic Lesion ◽  
Foam Cell Formation ◽  
Acid Oxidation ◽  
Fatty Acid Binding ◽  
Apoe Knockout Mice

The transcription factor NF-κB p65 is a key regulator in the regulation of an inflammatory response and in the pathology of atherosclerosis. However, there is no direct evidence for the role of NF-κB in macrophages in the development of atherosclerosis. We investigated whether macrophage overexpression of p65 in apoE-knockout mice could improve atherosclerosis. Transgenic (Tg) mice overexpressing p65 in macrophages were generated by crossing fatty acid-binding protein 4 (aP2) promoter-controlled p65 mice with apoE-knockout (KO) mice. Tg mice exhibited functional activation of NF-κB signaling in macrophages and fat tissues. We observed that the atherosclerotic lesion was 40% less in the Tg mice compared with the apoE-KO controls fed a standard atherogenic diet for 16 wk ( n = 12). The Tg mice were leaner from reduced fat mass by increased energy expenditure. Moreover, the overexpression of p65 in macrophages suppressed foam cell formation. Our results show that there is 1) an increased fatty acid oxidation in macrophages, 2) a reduced scavenger receptor CD36 expression and lipid accumulation in microphages, 3) reduced-inflammation cytokines in serum, and 4) enhanced energy expenditure in Tg mice. Our data suggest that activation of NF-κB in macrophages has atheroprotective effects in mice by enhancing lipid metabolism and energy expenditure.

scholarly journals Dulaglutide exerts beneficial anti atherosclerotic effects in ApoE knockout mice with diabetes: the earlier, the better

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Junpei Sanada ◽  
Atsushi Obata ◽  
Yoshiyuki Obata ◽  
Yoshiro Fushimi ◽  
Masashi Shimoda ◽  
...  
Keyword(s):  
Early Intervention ◽  
Knockout Mice ◽  
Aortic Root ◽  
Late Phase ◽  
Intervention Group ◽  
Atherosclerotic Lesion ◽  
Expression Levels ◽  
Late Intervention ◽  
Apoe Knockout Mice ◽  
Early Intervention Group

AbstractThere has been no report about the mechanism for anti-atherosclerotic effects of dulaglutide (Dula) and/or about the difference of its effectiveness between in an early and a late phase of diabetes. To address such questions, streptozotocin (STZ) was intraperitoneally injected to ApoE knockout mice at 8 weeks of age. Either Dula or vehicle was administered to STZ-induced diabetic ApoE knockout mice from 10 to 18 weeks of age as an early intervention group and from 18 to 26 weeks as a late intervention group. Next, non-diabetic ApoE knockout mice without STZ injection were subcutaneously injected with either Dula or vehicle. In an early intervention group, atherosclerotic lesion in aortic arch and Mac-2 and CD68-positive areas in aortic root were significantly smaller in Dula group. In abdominal aorta, expression levels of some villain factors were lower in Dula group. In a late intervention group, there were no immunohistological differences in aortic root and expression levels of various factors between two groups. Furthermore, even in non-diabetic ApoE knockout mice, expression levels of inflammatory and macrophage markers were reduced by treatment with Dula. Taken together, Dula exerts more beneficial anti-atherosclerotic effects in an early phase of diabetes rather than in a late phase.

scholarly journals Effects of compound-326, a selective delta-5 desaturase inhibitor, in ApoE knockout mice with two different protocols for atherosclerosis development

2021 ◽  
Vol 24 ◽  
pp. 71-83
Author(s):  
Hiroki Nagase ◽  
Shuichi Takagahara ◽  
Yoshinori Satomi ◽  
Ayumi Ando ◽  
Kazuki Kubo ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Treatment Protocol ◽  
Atherosclerotic Lesion ◽  
Western Diet ◽  
Intercellular Adhesion Molecule ◽  
Lesion Area ◽  
Apoe Knockout Mice ◽  
Pre Treatment ◽  
Atherosclerosis Development ◽  
Delta 5 Desaturase

Purpose: We previously confirmed its anti-atherosclerotic effects by pre-treatment with compound-326, a selective delta-5 desaturase (D5D) inhibitor, in Western diet-fed ApoE knockout mice. In the present study, we evaluated effects of compound-326 in ApoE knockout mice with two different protocols for atherosclerosis development. Methods: In a post-treatment protocol, where the compound treatment started after 10 weeks pre-feeding of Western diet, compound-326 (1 and 3 mg/kg/day, p.o. for 12 weeks) significantly reduced the atherosclerotic lesion area in the aorta (24% reduction at 3 mg/kg/day). In another protocol using Paigen diet (containing 12.5% cholesterol and 5% sodium cholate), compound-326 (3 and 10 mg/kg/day, p.o. for 7 weeks) also significantly reduced the lesion area (36% reduction at 3 mg/kg/day). Results: In both protocols, Compound-326 significantly reduced the hepatic ratio of arachidonic acid to dihomo-γ-linolenic acid, blood inflammatory eicosanoid production and plasma soluble intercellular adhesion molecule 1 (sICAM-1) levels, similarly to the previous pre-treatment study. Conclusions: Compound-326 exerted anti-atherosclerotic effects in ApoE knockout mice with the two different protocols for atherosclerosis development further supporting D5D inhibition as a promising strategy in treating atherosclerosis.

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