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Updated: Jul 18, 2026
Isolation of Murine Coronary Vascular Smooth Muscle Cells
Published on: May 30, 2016
Modulation of CD36 protein expression by AGEs and insulin in aortic VSMCs from diabetic and non-diabetic rats
Cristina de Oliveira Silva1, Sandrine Delbosc, Caroline Araïs
1Laboratoire de Nutrition Humaine et Athérogénèse (LNHA), EA 2993, Institut Universitaire de Recherche Clinique, Université Montpellier I, 641 Avenue du Doyen Giraud, 34093 Montpellier, France. cos@montp.inserm.fr
Background And Aim:
In type 2 diabetes, the interplay between cells and inflammatory mediators up-regulates CD36 expression in macrophages. The aim of this work was to investigate advanced glycation end products (AGE)-induced CD36 expression and its regulation by insulin in aortic vascular smooth muscle cells (VSMCs) from Goto-Kakisaki (GK) rats, a non-obese insulin model of both insulin resistance and type 2 diabetes. The context of overexpression of CD36 in aortas was also evaluated.
Methods And Results:
VSMCs were isolated and cultured from the aortas of GK rats and non-diabetic rats. The expression of proteins was evaluated by Western blot. The aortic production of superoxide anion (O(2)(.-)) was measured by luminescence on isolated tissue. AGEs and advanced oxidation protein products (AOPPs) were determined in plasma by fluorescence spectroscopy and spectrophotometry, respectively. AGE receptor (RAGE), NF-kappaB, and CD36 protein expression as well as O(2)(.-) production were higher in GK aortas than in control aortas, and AGEs and AOPPs were higher in GK plasma. In VSMCs from non-diabetic rats, insulin was able to reduce (10 nM) or suppress (100 nM) the protein overexpression of CD36 induced by AGEs-BSA. In contrast, in VSMCs from GK rats, insulin was unable to reduce AGEs-BSA-induced CD36 overexpression.
Conclusions:
The results suggest an overexpression of CD36 in VSMCs from GK rats and impaired control by insulin. In the context of increased plasma AGEs, aortic RAGE overexpression and increased oxidative stress markers, the data are compatible with an AGEs induced CD36 overexpression in diabetes.
