Cited by 169Advanced Glycation End Products researchNitric Oxide and Endothelin EffectsParathyroid Disorders and Treatments

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Calcitriol blunts the deleterious impact of advanced glycation end products on endothelial cells

Talmor, Yeela, Golan, Eliezer, Benchetrit, Sydney, Bernheim, Jacques, Klein, Osnat, Green, Janice, Rashid, Gloria·2008·American Journal of Physiology-Renal Physiology

DOI 10.1152/ajprenal.00051.2008

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Abstract

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-kappaB 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-kappaB-p65 DNA binding activity was enhanced and associated with a decrease in inhibitor kappaBalpha (IkappaBalpha) and an increase in phosphorylated (p)-IkappaBalpha levels. Addition of calcitriol blunted the AGEs-induced elevation of NF-kappaB-p65 DNA binding activity, a phenomenon related to an increased expression of IkappaBalpha. This increase was correlated to declined p-IkappaBalpha 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.

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Authors: Talmor, Y., Golan, E., Benchetrit, S., Bernheim, J., Klein, O., Green, J., & Rashid, G.
Venue: American Journal of Physiology-Renal Physiology
Publisher: American Physiological Society
Published: 2008-05
Volume: 294
Issue: 5
Pages: F1059-F1064
ISSN: 1522-1466 (ISSN-L)
1931-857X
DOI: 10.1152/ajprenal.00051.2008
OpenAlex: W2137927685
Cited by: 169
References: 40
Citations by year: 2026: 4 · 2025: 5 · 2024: 3 · 2023: 3 · 2022: 7 · 2021: 4 · 2020: 10 · 2019: 12 · 2018: 9 · 2017: 17 · 2016: 9 · 2015: 14 · 2014: 15 · 2013: 9 · 2012: 8
FWCI: 8.91
Type: journal article
Language: en
Open access: closed
Locations: American Journal of Physiology-Renal Physiology (publishedVersion)
PubMed (publishedVersion)
Funders: Abbott Laboratories
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
Keywords: 1,25-dihydroxyvitamin D3, advanced glycation end products, endothelial cells, endothelial nitric oxide synthase, NF-κB, IκBα, AGE receptor, interleukin-6, vascular dysfunction, diabetic vascular complications, uremia
MeSH terms: Receptor for Advanced Glycation End Products, Calcitriol, Calcium Channel Agonists, Cells, Cultured, Humans, Inflammation, Receptors, Immunologic, RNA, Serum Albumin, Bovine, Blotting, Western, Signal Transduction, Interleukin-6, NF-kappa B, Glycation End Products, Advanced, Reverse Transcriptase Polymerase Chain Reaction, Endothelial Cells, Nitric Oxide Synthase Type III

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Calcitriol blunts the deleterious impact of advanced glycation end products on endothelial cells

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