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Speid, W.S., Kastl, S.P., Hutter, R., Katsaros, K.M., Kaun, C., Bauriedel, G., Maurer, G., Huber, K., Badimon, J.J. and Wojta, J. (2011) The Complement Component C5a Is Present in Human Coronary Lesions in Vivo and Induces the Expression of MMP-1 and MMP-9 in Human Macrophages in Vitro. FASEB Journal, 25, 35-44.
http://dx.doi.org/10.1096/fj.10-156083

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