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Tous, M., Ferré, N., Rull, A., Marsillach, J., Coll, B., Alonso-Villaverde, C., Camps, J. and Joven, J. (2006) Dietary Cholesterol and Differential Monocyte Chemoattractant Protein-1 Gene Expression in Aorta and Liver of Apo E-Deficient Mice. Biochemical and Biophysical Research Communications, 340, 1078-1084.
http://dx.doi.org/10.1016/j.bbrc.2005.12.109

has been cited by the following article:

• TITLE: C5L2 Deficiency Enhances Development of Atherosclerosis in ApoE Knockout Mice

  AUTHORS: Yan Liu, Alexandre Fisette, Marc Lapointe, Katherine Cianflone

  KEYWORDS: Atherosclerosis, C5L2, Inflammation, Metabolism, Lipid, Glucose

  JOURNAL NAME: Chinese Medicine, Vol.6 No.1, March 26, 2015

  ABSTRACT: Background: The complement system is important in development of atherosclerosis via regulation of lipid and glucose metabolism as well as inflammation. Aim: The aim of the present study was to further analyze the contribution of C5L2 to the development of atherosclerosis. We proposed that, with DIO feeding, C5L2 deficiency would promote a phenotype that encourages atherosclerosis development. Coupled to ApoE deficiency, double knockout (2KO) mice would show exacerbated atherosclerotic plaque formation. Methods: First, Wildtype (WT) and C5L2-/-(C5L2KO) and subsequently, ApoE-/-(ApoEKO) and C5L2/ApoE double knockout mice were placed on diets inducing obesity (DIO) or standard chow diet for 12 - 15 weeks. Plasma lipids, glucose, cytokines and hepatic glycogen and lipid contents, mRNA levels and enzyme activities and atherosclerotic plaque size were measured. Results: C5L2KO had increased hepatic glucose oxidation (+90%, p