Experimental Model of Atherosclerosis with Lesions in Aorto-iliac Axis in ApoE -/- Mice
Author(s)
Luis Riera del Moral , Alexia Paluso Montero , Carlota Largo Aramburu , Teresa Vallejo Cremades , Teresa Hernández Ruiz ,
Download Full PDF Pages: 12-18 | Views: 719 | Downloads: 133 | DOI: 10.5281/zenodo.4576980
Volume 10 - February 2021 (02)
Abstract
Introduction: Atherosclerosis is an inflammatory chronic disease which has an elevated prevalence. The mouse model is the most commonly used.
Materials and methods: An experimental and descriptive study of a group of 20 male mice C57BL/6J KO apoE -/- fed high-fat diet during 14 weeks was carried out. Analysis of the aorto-iliac axis and the presence of advanced atherosclerotic lesions affecting the subjects, as well as levels of triglycerids and total cholesterol. Weight of each subject was measured every week.
Results: There is a global tendency in all the subjects to gain weight and have higher levels of triglycerids and total cholesterol at the end of the study. Most subjects developed advanced atherosclerotic lesions in histological samples.
Discussion: Most studies have analyzed lesions in aortic root, but these don´t allow to know the severity of the disease. In the same line as other studies, we have successfully obtained atherosclerotic lesions.
Conclusions: This experimental model with genetically modified mice provides the development of advanced atherosclerotic lesions in the aorto-iliac axis after high-fat diet during 14 weeks and a correlation with alteration of the lipoprotein profile in plasma.
Keywords
Experimental Model, Atherosclerosis, Aorto-Iliac Axis
References
i. Bonow RO, Smaha LA, Smith SC, Mensah GA, Lenfant C. World Heart Day 2002: The international burden of cardiovascular disease: Responding to the emerging global epidemic. Circulation. 2002;
ii. Lusis AJ. Atherosclerosis. Nature. 2000.
iii. Santos-Gallego CG, Badimon JJ, Ibáñez B. Modelos experimentales de aterosclerosis. Rev Esp Cardiol Supl. 2013;
iv. Navarro MA, Arbonés JM, Acín S, Carnicer R, Sarría AJ, Surra JC, et al. Animales de experimentación utilizados como modelos en la investigación de la arteriosclerosis. Clínica e Investig en Arterioscler. 2005;
v. Lin Y, Bai L, Chen Y, Zhu N, Bai Y, Li Q, et al. Practical assessment of the quantification of atherosclerotic lesions in apoE-/- mice. Mol Med Rep. 2015;
vi. Paigen B, Morrow A, Holmes PA, Mitchell D, Williams RA. Quantitative assessment of atherosclerotic lesions in mice. Atherosclerosis. 1987;
vii. Plump AS, Smith JD, Hayek T, Aalto-Setälä K, Walsh A, Verstuyft JG, et al. Severe hypercholesterolemia and atherosclerosis in apolipoprotein E-deficient mice created by homologous recombination in ES cells. Cell. 1992;
viii. Zhou Y, Chen R, Liu D, Wu C, Guo P, Lin W. Asperlin inhibits LPS-evoked foam cell formation and prevents atherosclerosis in ApoE−/−mice. Mar Drugs. 2017;15(11).
ix. Meir KS, Leitersdorf E. Atherosclerosis in the apolipoprotein E-deficient mouse: A decade of progress. Arteriosclerosis, Thrombosis, and Vascular Biology. 2004.
x. Tian Y, Liang X, Wu Y. The alternation of autophagy/apoptosis in CD4+CD25+Foxp3+ Tregs on the developmental stages of atherosclerosis. Biomed Pharmacother. 2018;97:1053–60.
xi. Zadelaar S, Kleemann R, Verschuren L, De Vries-Van Der Weij J, Van Der Hoorn J, Princen HM, et al. Mouse models for atherosclerosis and pharmaceutical modifiers. Arteriosclerosis, Thrombosis, and Vascular Biology. 2007.
xii. Tangirala RK, Rubin EM, Palinski W. Quantitation of atherosclerosis in murine models: Correlation between lesions in the aortic origin and in the entire aorta, and differences in the extent of lesions between sexes in LDL receptor-deficient and apolipoprotein E-deficient mice. J Lipid Res. 1995;
xiii. Getz GS, Reardon CA. Diet and murine atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology. 2006.
Cite this Article: