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Rodriguez-Lee, M., Ostergren-Lunden, G., Wallin, B., Moses, J., Bondjers, G. and Camejo, G. (2006) Fatty acids cause alterations of human arterial smooth muscle cell proteoglycans that increase the affinity for low-density lipoprotein. Arteriosclerosis, Thrombosis, and Vascular Biology, 26, 130-135. http://dx.doi.org/10.1161/01.ATV.0000191659.94059.62

has been cited by the following article:

• TITLE: Adipocytes modulate vascular smooth muscle cells migration potential through their secretions

  AUTHORS: Souhad El Akoum, Isabelle Cloutier, Jean-François Tanguay

  KEYWORDS: Adipocytes; Atherosclerosis; Type 2 Diabetes; Vascular Smooth Muscle Cells; Migration

  JOURNAL NAME: Journal of Diabetes Mellitus, Vol.3 No.4, November 26, 2013

  ABSTRACT: Impairment of vascular smooth muscle cells (VSMC) is recognized as a predisposition factor for atherosclerosis development. We hypothesize that the metabolic syndrome has a direct impact on VSMC migration and phenotypic switching, which may increase the incidence of atherosclerotic events. Aortic VSMC were extracted from 10 weeks old C57BL6 mice and incubated for 24 hr in adipocytes conditioned cell culture medium. Adipocytes were extracted from diabetic C57BL6 male mice fed with either a vegetal or an animal High-Fat-Diet (HFD) for 20 weeks. Migration of VSMC in response to conditioned media stimulations was significantly modulated compared to control. The most extended effects on VSMC were triggered by adipocytes from mice fed with animal HFD. These effects were concurrent with increased leptin concentrations and decreased adiponectin levels in conditioned media. A significant up-regulation of CD36 mRNA level was found in VSMC treated with adipocytes from HFD-fed mice. In conclusion, we have shown that the development of adipocyte-induced VSMC alterations is linked to diet fatty acid composition and the degree of metabolic alterations. The modulation of adipokine secretions in the adipose tissue that is linked to metabolic alterations may alter the physiology of VSMC and thus accelerate the development of metabolic-related vascular diseases.