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.
Highlights
Obesity and type 2 diabetes (T2D) are recognized as predisposition factors for atherosclerosis development
To characterize the effect of these modulations on vascular smooth muscle cells (VSMC), abdominal adipocytes were isolated from each animal group and used to condition culture media
The current study appears to be compelling, and makes a significant contribution to the field of atherogenesis process as well as the understanding of the impact of the adipose tissue on VSMC. It reflects the direct impact of adipose tissue secretion cocktail on the VSMC migratory potential; and it’s a main characteristic that affects atherogenesis
Summary
Obesity and type 2 diabetes (T2D) are recognized as predisposition factors for atherosclerosis development. At the early stage of atherogenesis, the oxLDL-exposed endothelium becomes activated and up-regulates the expression of adhesion molecules (ICAM, VCAM), thereby allowing monocyte recruitment and initiation of the inflammatory process [4]. For their part, VSMC undergo “phenotypic switching”, which is characterized by decreased contractibility and increased proliferation and migration toward the intima. VSMC may undergo cholesterol-induced trans-differentiation into foam cells [7] These cells have a macrophage like phenotype and express increased levels of the oxLDL scavenger receptor CD36, which favors lipid accumulation and contributes to the atherogenic process [8]
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