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Am J Physiol Renal Physiol 294: F1059-F1064, 2008. First published March 19, 2008; doi:10.1152/ajprenal.00051.2008
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Calcitriol blunts the deleterious impact of advanced glycation end products on endothelial cells

Yeela Talmor,1,2 Eliezer Golan,1,2 Sydney Benchetrit,1,2 Jacques Bernheim,1,2 Osnat Klein,1,2 Janice Green,1 and Gloria Rashid1

1Renal Physiology Laboratory, Department of Nephrology and Hypertension, Meir Medical Center, Kfar-Saba and 2Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

Submitted 29 January 2008 ; accepted in final form 17 March 2008

Advanced glycation end products (AGEs), which are elevated in diabetic and uremic patients, may induce vascular dysfunctions, and calcitriol may improve the cardiovascular complications. Therefore, we examined whether calcitriol may modify the endothelial response to AGEs stimulation. Knowing the importance of nuclear factor-{kappa}B in endothelial inflammatory responses, the effect of AGEs and calcitriol on this pathway was also studied. Calcitriol was added to endothelial cells previously incubated with AGE-human serum albumin (HSA). AGE-HSA induced a decrease in endothelial nitric oxide synthase (eNOS) mRNA expression and enzyme activity. Addition of calcitriol to AGE-HSA-treated endothelial cells improved the decreased action of AGEs on the eNOS system. AGE-HSA increased the AGEs receptor mRNA and protein, which were both blunted by calcitriol. The parallel elevation of interleukin-6 mRNA in the presence of AGE-HSA was also blunted by calcitriol. The NF-{kappa}B-p65 DNA binding activity was enhanced and associated with a decrease in inhibitor {kappa}B{alpha} (I{kappa}B{alpha}) and an increase in phosphorylated (p)-I{kappa}B{alpha} levels. Addition of calcitriol blunted the AGEs-induced elevation of NF-{kappa}B-p65 DNA binding activity, a phenomenon related to an increased expression of I{kappa}B{alpha}. This increase was correlated to declined p-I{kappa}B{alpha} levels. The present results support the concept that calcitriol may act as a vascular protective agent counteracting the probable deleterious actions of AGEs on endothelial cell activities.

vitamin D; advanced glycation end products; nuclear factor-{kappa}B; endothelial cells


Address for reprint requests and other correspondence: G. Rashid, Renal Physiology Laboratory, Dept. of Nephrology and Hypertension, Meir Medical Center, Kfar-Saba, Tchernichovsky 59, Kfar-Saba 44281, Israel (e-mail: Gloriar{at}clalit.org.il)






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