Accordingly, results from hematoxylin and eosin staining, western blotting and immunofluorescence staining demonstrated that β‑glucan accelerated the progress of atherosclerosis in apolipoprotein E‑deficient mice and modulated expression of dectin‑1, beclin‑1 and light chain 3II/I in aortas similarly to that observed in macrophages.
Recently, APOE-knockout in rabbits has been shown to promote atherosclerosis and associated premature IVD degeneration that mimic the symptoms of atherosclerosis and structural changes of IVDs in humans.
The aim of this review was to investigate the potential underlying mechanisms related to APOE4 that could increase the risk of periodontal disease and, ultimately, of atherosclerosis.
In the present study, atherosclerosis model was developed using apolipoprotein E-deficient mice that was treated with long-term high-fat food and chronic stresses.
Alcohol Consumption in Combination with an Atherogenic Diet Increased Indices of Atherosclerosis in Apolipoprotein E/Low-Density Lipoprotein Receptor Double-Knockout Mice.
To generate novel rabbit models with a large-fragment deletion of either LDL receptor (LDLR) and/or apolipoprotein (apoE) genes for the study of hyperlipidemic and atherosclerosis.
Recently, we demonstrated that progerin-driven vascular smooth muscle cell (VSMC) loss accelerates atherosclerosis leading to premature death in apolipoprotein E-deficient mice.
In this study, we collected blood samples from patients of coronary artery diseases and apolipoprotein E (ApoE)<sup>-/-</sup> mice that were fed a Western diet for 12 wk to induce atherosclerosis and found that serum CTRP13 level was decreased.
Western blot and fluorescence-activated cell sorting analysis showed that Rheb expression was significantly increased in atherosclerotic lesions of atherosclerosis-prone (apoE<sup>-/-</sup> [apolipoprotein E deficient]) mice fed with Western diet.
Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)-/- mice.
Our aim was to investigate the potential role of a ClC-2 chloride channel activator, lubiprostone, which is reported to have beneficial effects on LGS, in the development of atherosclerosis in apolipoprotein E-deficient (ApoE-/-) mice.
We investigated whether an increased type 2 polarization by administration of <i>Litomosoides sigmodontis</i> adult worm extract (LsAg) affects atherosclerosis in apolipoprotein E-deficient (ApoE<sup>-/-</sup>) mice.Injections of 50 µg LsAg, i.p. into ApoE<sup>-/-</sup> mice induced a type 2 immune response shown by increased frequencies of peritoneal eosinophils and alternatively activated macrophages.
Hereto, regular chow diet-fed atherosclerosis-susceptible hypercholesterolemic apolipoprotein E (APOE) knockout mice were treated with the bile duct toxicant alpha‑naphthylisothiocyanate (ANIT) for 8 weeks.
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.