1α,25-dihydroxycholecalciferol induces nitric oxide production in cultured endothelial cells.

Détails

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Accès restreint UNIL
Etat: Public
Version: Final published version
Licence: Non spécifiée
ID Serval
serval:BIB_0583C4C8E65D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
1α,25-dihydroxycholecalciferol induces nitric oxide production in cultured endothelial cells.
Périodique
Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
Auteur⸱e⸱s
Molinari C., Uberti F., Grossini E., Vacca G., Carda S., Invernizzi M., Cisari C.
ISSN
1421-9778 (Electronic)
ISSN-L
1015-8987
Statut éditorial
Publié
Date de publication
2011
Peer-reviewed
Oui
Volume
27
Numéro
6
Pages
661-668
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
Résumé
BACKGROUND: Recently, 1α,25-dihydroxycholecalciferol (vitD) has received increasing interest for its effects on many tissues and organs other than bone. A number of experimental studies have shown that vitD may have an important role in modifying risk for cardiovascular disease.
AIMS: This study was planned to test the effects of vitD on endothelial nitric oxide (NO) production and to study the intracellular pathways leading to NO release.
METHODS: In human umbilical vein endothelial cells (HUVEC) cultures the effects of vitD on NO production and p38, Akt, ERK and eNOS phosphorylations were examined in absence or in presence of the NO synthase inhibitor L-NAME and protein kinases specific inhibitors SB203580, wortmannin and UO126.
RESULTS: VitD caused a concentration-dependent increase in NO production. The maximum effect was observed at a concentration of 1 nM and the optimal time of stimulation was 1 min. Effects induced by vitD were abolished by L-NAME and by pre-treatment with protein kinases inhibitors. To verify the effective involvement of vitD receptor (VDR) in the action mechanism of vitD, experiments were repeated in presence of the specific VDR ligands ZK159222 and ZK191784.
CONCLUSIONS: The results of this study demonstrate that vitD can induce a significant increase in endothelial NO production. VitD interaction with VDR caused the phosphorylation of p38, AKT and ERK leading to eNOS activation.
Mots-clé
Blotting, Western, Cells, Cultured, Dihydroxycholecalciferols/pharmacology, Endothelium, Vascular/cytology, Endothelium, Vascular/metabolism, Humans, Nitric Oxide/biosynthesis
Pubmed
Open Access
Oui
Création de la notice
25/03/2013 17:16
Dernière modification de la notice
15/07/2020 5:26
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