scholarly journals Advanced Glycation End-Products Induce Apoptosis of Vascular Smooth Muscle Cells: A Mechanism for Vascular Calcification

2016 ◽  
Vol 17 (9) ◽  
pp. 1567 ◽  
Author(s):  
Sayo Koike ◽  
Shozo Yano ◽  
Sayuri Tanaka ◽  
Abdullah Sheikh ◽  
Atsushi Nagai ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Calcification ◽  
Vascular Smooth Muscle Cells ◽  
Advanced Glycation End Products ◽  
Muscle Cells ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals Advanced Glycation End-products Enhance Calcification in Vascular Smooth Muscle Cells

2009 ◽  
Vol 37 (3) ◽  
pp. 847-854 ◽  
Author(s):  
X Ren ◽  
H Shao ◽  
Q Wei ◽  
Z Sun ◽  
N Liu
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Calcification ◽  
Vascular Smooth Muscle Cells ◽  
Advanced Glycation End Products ◽  
Muscle Cells ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

Advanced glycation end-products (AGEs), senescent macroprotein derivatives formed at an accelerated rate in diabetes, are closely associated with vascular calcification in humans. In this study, the hypothesis that AGEs enhance calcification in cultured vascular smooth muscle cells (VSMCs) was tested. Using real-time polymerase chain reaction (PCR) and specific protein assays, it was demonstrated that rat aortic VSMCs incubated with AGEs exhibited an increased expression of the AGE receptor (RAGE) and typical bone proteins, such as osteopontin and alkaline phosphatase. Incubation with AGEs also enhanced calcium accumulation in VSMCs in time-and dose-dependent manners. These AGEs-mediated changes in VSMCs were partially attenuated by a neutralizing antibody to RAGE. The results suggest that AGEs that accumulate in diabetes could elicit the osteoblastic differentiation of VSMCs, thereby contributing to vascular calcification via the RAGE pathway. Interruption of the AGE-RAGE interaction might be a promising target for therapeutic intervention to prevent diabetic vascular calcification.

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