AJP - Renal Add DOIs to your references at manuscript stage!
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol 294: F1059-F1064, 2008. First published March 19, 2008; doi:10.1152/ajprenal.00051.2008
0363-6127/08 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
294/5/F1059    most recent
00051.2008v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Talmor, Y.
Right arrow Articles by Rashid, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Talmor, Y.
Right arrow Articles by Rashid, G.

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)






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.