scholarly journals Advanced glycation end products promote human aortic smooth muscle cell calcification in vitro via activating NF-κB and down-regulating IGF1R expression

2013 ◽  
Vol 34 (4) ◽  
pp. 480-486 ◽  
Author(s):  
Yi Wang ◽  
Zhen-yu Zhang ◽  
Xiao-qing Chen ◽  
Xiang Wang ◽  
Heng Cao ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Advanced Glycation End Products ◽  
Aortic Smooth Muscle Cell ◽  
Advanced Glycation ◽  
Aortic Smooth Muscle ◽  
Glycation End Products ◽  
End Products ◽  
Igf1r Expression

scholarly journals Advanced Glycation End Products Induce Vascular Smooth Muscle Cell-Derived Foam Cell Formation and Transdifferentiate to a Macrophage-Like State

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Zhengyang Bao ◽  
Lihua Li ◽  
Yue Geng ◽  
Jinchuan Yan ◽  
Zhiyin Dai ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Advanced Glycation End Products ◽  
Foam Cell ◽  
Cell Formation ◽  
Foam Cell Formation ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

Background. Advanced glycation end products play an important role in diabetic atherosclerosis. The effects of advanced glycation end products (AGEs) on vascular smooth muscle cell- (VSMC-) derived foam cell formation and phenotypic transformation are unknown. Methods. Serological and histological samples were obtained from diabetic amputation patients and accident amputation patients from the Affiliated Hospital of Jiangsu University. CD68/Actin Alpha 2 (ACTA2) coimmunofluorescence sections were used to quantify the number of VSMCs with macrophage-like phenotypes. Western blotting was used to detect the expression of the receptor of advanced glycation end products in vascular samples. Enzyme-linked immunosorbent assay (ELISA) was used to evaluate the level of serum Nε-carboxymethyl-lysine (CML). In vitro oil red O staining was used to examine lipid accumulation in VSMCs stimulated by CML. The expression of VSMCs and macrophage markers was measured by western blotting and quantitative real-time PCR. Furthermore, changes in VSMC migration and secretion were detected by the Transwell assay and ELISA. Results. In the arterial plaque sections of diabetic patients, VSMCs transformed to a macrophage-like phenotype. The serum CML and RAGE levels in the plaques were significantly higher in the diabetes group than those in the healthy control group and were significantly related to the number of macrophage-like VSMCs. CML stimulation promoted intracellular lipid accumulation. However, CML stimulation decreased the expression of VSMC markers and increased the expression of macrophage phenotype markers. Finally, CML promoted smooth muscle cell migration and the secretion of proinflammatory-related factors. Conclusions. CML induces VSMC-derived foam cell formation, and VSMCs transdifferentiate to a macrophage-like state, which may be mediated by the activation of RAGE.

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