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Nephrol Dial Transplant. 2009 Nov;24(11):3306-12. doi: 10.1093/ndt/gfp354. Epub 2009 Jul 18.

Low extracellular Ca2+: a mediator of endothelial inflammation.

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

Abstract

BACKGROUND:

Recent studies have suggested that vitamin D and an imbalance in calcium homeostasis may have an impact on the cardiovascular system. The aim of this study was to assess the impact of different concentrations of extracellular Ca(2+) on human umbilical vein cord endothelial cells (HUVEC) by measuring its effect on parameters involved in the pathogenesis of vascular inflammatory responses.

METHODS:

HUVEC were grown in the 3.5, 4.5 or 5.8 mg/dL concentration of extracellular Ca(2+) for 2-3 weeks. Expression of adhesion molecules was analysed by flow cytometry. Endothelial nitric oxide synthase (eNOS), receptor of advanced glycation end-product (RAGE) and interleukin-6 (IL-6) mRNA expressions were determined by real-time PCR. eNOS, inhibitor kappa Balpha (IkappaBalpha) and phosphorylated IkappaBalpha protein levels by Western blot, eNOS activity by conversion of [(14)C]-arginine to [(14)C]-citrulline, IL-6 and osteoprotegerin (OPG) secretion by ELISA and DNA-binding activity of nuclear factor kappa B (NFkappaB)-p65 were assayed colorimetrically in nuclear extracts.

RESULTS:

In the presence of low Ca(2+) (3.5 mg/dL), protein expressions and activity of eNOS were diminished, while the protein expressions of intercellular adhesion molecule-1 (ICAM-1), as well as the mRNA expressions of RAGE and IL-6, were elevated. The protein secretions of IL-6 and OPG were also stimulated in low Ca(2+) concentration. At this concentration, the DNA-binding activity of NFkappaB was enhanced, probably due to the decreased level of IkappaBalpha.

CONCLUSIONS:

These results suggest that lower extracellular ionized Ca(2+) may play a relevant role in modifying endothelial cells functions.

PMID:
19617602
DOI:
10.1093/ndt/gfp354
[PubMed - indexed for MEDLINE]
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