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Dietary Vitamin D and Its Metabolites Non-Genomically Stabilize the Endothelium

Gibson, Christopher C ; Davis, Chadwick T ; Zhu, Weiquan ; Bowman-Kirigin, Jay A ; Walker, Ashley E ; Tai, Zhengfu ; Thomas, Kirk R ; Donato, Anthony J ; Lesniewski, Lisa A ; Li, Dean Y Slominski, Andrzej T

PloS one, 2015-10, Vol.10 (10), p.e0140370-e0140370 [Periódico revisado por pares]

United States: Public Library of Science

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Título:
Dietary Vitamin D and Its Metabolites Non-Genomically Stabilize the Endothelium
Autor: Gibson, Christopher C ; Davis, Chadwick T ; Zhu, Weiquan ; Bowman-Kirigin, Jay A ; Walker, Ashley E ; Tai, Zhengfu ; Thomas, Kirk R ; Donato, Anthony J ; Lesniewski, Lisa A ; Li, Dean Y
Slominski, Andrzej T
Assuntos: Alfacalcidol ; Animals ; Arthritis ; Biochemistry ; Bioengineering ; Calcifediol ; Calcitriol ; Capillary Permeability ; Cardiology ; Cardiovascular diseases ; Care and treatment ; Cells, Cultured ; Cholecalciferol - analogs & derivatives ; Cholecalciferol - pharmacology ; Chronic obstructive pulmonary disease ; Cytokines ; Diet ; Disease ; Endocrinology ; Endothelial cells ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Endothelium ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Geriatrics ; Health aspects ; Health risks ; Homeostasis ; Humans ; Inflammation ; Inflammatory diseases ; Laboratories ; Medicine ; Metabolites ; Mice ; Molecular biology ; Multiple sclerosis ; Pharmaceuticals ; Risk factors ; Salt ; Sepsis ; Serum levels ; Stability ; Systemic lupus erythematosus ; Transcription ; Vitamin D ; Vitamin D3 ; Vitamin deficiency ; Vitamins - pharmacology
É parte de: PloS one, 2015-10, Vol.10 (10), p.e0140370-e0140370
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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Competing Interests: The authors have the following interests. The University of Utah has licensed 'know how' related to this manuscript to Recursion Pharmaceuticals, a biotechnology company owned in part by the University of Utah Research Foundation. Christopher C. Gibson and Dean Y. Li are co-founders of Recursion Pharmaceuticals, while Chadwick T. Davis and Kirk R. Thomas are employed by Recursion Pharmaceuticals. Christopher C. Gibson, Chadwick T. Davis, Kirk R. Thomas and Dean Y. Li have real or optional ownership interest in Recursion. There are no further patents, products in development or marketed products to declare. This does not alter the authors’ adherence to all the PLOS ONE policies on sharing data and materials, as detailed online in the guide for authors.
Conceived and designed the experiments: CCG CTD KRT LAL AJD DYL. Performed the experiments: CCG CTD WZ JAB-K AEW ZT. Analyzed the data: CCG CTD WZ JAB-K AEW. Contributed reagents/materials/analysis tools: DYL LAL AJD. Wrote the paper: CCG CTD KRT DYL.
Descrição: Vitamin D is a known modulator of inflammation. Native dietary vitamin D3 is thought to be bio-inactive, and beneficial vitamin D3 effects are thought to be largely mediated by the metabolite 1,25(OH)2D3. Reduced serum levels of the most commonly measured precursor metabolite, 25(OH)D3, is linked to an increased risk of multiple inflammatory diseases, including: cardiovascular disease, arthritis, multiple sclerosis, and sepsis. Common to all of these diseases is the disruption of endothelial stability and an enhancement of vascular leak. We previously performed an unbiased chemical suppressor screen on a genetic model of vascular instability, and identified cholecalciferol (D3, dietary Vitamin D3) as a factor that had profound and immediate stabilizing and therapeutic effects in that model. In this manuscript we show that the presumed inactive sterol, D3, is actually a potent and general mediator of endothelial stability at physiologically relevant concentrations. We further demonstrate that this phenomenon is apparent in vitamin D3 metabolites 25(OH)D3 and 1,25(OH)2D3, and that the effects are independent of the canonical transcription-mediated vitamin D pathway. Our data suggests the presence of an alternative signaling modality by which D3 acts directly on endothelial cells to prevent vascular leak. The finding that D3 and its metabolites modulate endothelial stability may help explain the clinical correlations between low serum vitamin D levels and the many human diseases with well-described vascular dysfunction phenotypes.
Editor: United States: Public Library of Science
Idioma: Inglês

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Dietary Vitamin D and Its Metabolites Non-Genomically Stabilize the Endothelium

Gibson, Christopher C ; Davis, Chadwick T ; Zhu, Weiquan ; Bowman-Kirigin, Jay A ; Walker, Ashley E ; Tai, Zhengfu ; Thomas, Kirk R ; Donato, Anthony J ; Lesniewski, Lisa A ; Li, Dean Y Slominski, Andrzej T

United States: Public Library of Science

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