The aim of the current study is to characterize the interleukin 25 (IL25)-induced splenic ILC2 population (Lin<sup>-</sup>CD45<sup>+</sup>IL17RB<sup>+</sup>ICOS<sup>+</sup>IL7ra<sup>intermediate</sup>) and address its direct role in experimental atherosclerosis by its adoptive transfer to hypercholesterolaemic apolipoprotein E deficient (apoE<sup>-/-</sup>) mice.
Atherosclerosis-prone apolipoprotein E-deficient (ApoE-/-) mice which accumulate cholesterol ester-enriched particles in the blood due to poor lipoprotein clearance capacity were used as the atherosclerosis model in vivo.
Furthermore, oral administration of NATOH down-regulated NF-κB-dependent expression of pro-inflammatory markers (including IL-1β and adhesion molecules) and ameliorated atherosclerosis in Apo E knockout mice.
Most notably, Klotho deficiency is associated with a phenotype comprising organ manifestations accompanying aging including atherosclerosis and cognitive impairment.
Apolipoprotein E-deficient (ApoE<sup>-/-</sup>) mice develop atherosclerosis with severe PAH when fed a high-fat diet (HFD) and have increased levels of endothelin (ET)-1.
In the present study, we used Apolipoprotein E-deficient (ApoE<sup>-/-</sup>) mice model and in vitro cell line of RAW264.7 to explore the mechanisms of ethanol extracts of Danlou tablet (EEDT) in treating atherosclerosis.
In an atherosclerosis model established in apolipoprotein E-deficient mice, PNP encapsulating rapamycin significantly attenuated the progression of atherosclerosis and stabilized atherosclerotic plaques.
This suggests that eNOS deficiency may elevate aggrecan expression, which promotes apoptosis in VSMC, thereby contributing to atherosclerosis progression.
We investigated associations of APOE status with arteriolosclerosis, macroinfarcts and microinfarcts, and atherosclerosis in 1383 adults (65.9-108.2 years at death) with and without dementia.
For this purpose, 12-week old hyperlipidemic apolipoprotein E knockout mice were fed a Western-type diet for six weeks to induce both hepatic steatosis and atherosclerosis.
In line with these in vitro observations, in the atherosclerosis-susceptible apolipoprotein E (ApoE) KO background, CPT2 M-KO mice demonstrated augmented atherosclerosis, accompanied by increased accumulation of aortic macrophages with elevated CD36 expression.
Mice with double deletion in ARHGAP 18 and apolipoprotein E and fed a high-fat diet show early onset of atherosclerosis, with lesions developing in atheroprotective regions.
In parallel, apolipoprotein E-deficient (ApoE<sup>-/-</sup>) mice received a high-fat, high-cholesterol diet to induce atherosclerosis for 8 weeks, after which ApoE<sup>-/-</sup> mice received 300 <i>μ</i>g/kg of Lir daily or vehicle control for a further 4 weeks to investigate the attenuation of atherosclerosis.
In the apolipoprotein E-deficient mice, lentiviral expression of CTRP9 could suppress the atherosclerosis development, which could be abolished by AMPK inhibition.
The mouse model of accelerated atherosclerosis in lupus (gld.apoE<sup>-</sup><sup>/</sup><sup>-</sup> mouse) was generated from apolipoprotein E-deficient (apoE<sup>-</sup><sup>/</sup><sup>-</sup> ) and Fasl<sup>gld</sup> C57BL/6 mice.
<i>In vivo</i> experiments were performed in 2-mo-old atherosclerosis-prone apolipoprotein E-deficient/LDL receptor-deficient (ApoE<sup>-/-</sup>/LDLR<sup>-/-</sup>) female mice and their wild-type C57BL/6J littermates.