“…The mechanism by which 1,25-(OH) 2 D 3 mediated asthmatic airway remodeling was not fully elucidated. It has been shown that the VDR could interfere with the NF-κB p65 subunit and reduce the levels of IκBα protein, which directly results in its regulation of NF-κB activation (30)(31)(32)(33). 1,25-(OH) 2 D 3 binding to the VDR has been shown to regulate NF-κB activation and also modulate multiple biological activities both in vivo and in vitro (34)(35)(36)(37)(38)(39).…”
“…The mechanism by which 1,25-(OH) 2 D 3 mediated asthmatic airway remodeling was not fully elucidated. It has been shown that the VDR could interfere with the NF-κB p65 subunit and reduce the levels of IκBα protein, which directly results in its regulation of NF-κB activation (30)(31)(32)(33). 1,25-(OH) 2 D 3 binding to the VDR has been shown to regulate NF-κB activation and also modulate multiple biological activities both in vivo and in vitro (34)(35)(36)(37)(38)(39).…”
“…Metabolites of vitamin D further modify the physiology of nonskeletal tissues and, thus, regulate a wide array of biological functions [3,4]. 1,25(OH) 2 D 3 activates various signaling cascades via the vitamin D receptor which plays a decisive role in a myriad of cellular functions such as cell proliferation and differentiation, membrane transport, redox balance, adhesion, hemostasis and apoptosis [3][4][5][6][7]. Formation of 1,25(OH) 2 D 3 is down-regulated by fibroblast growth factor 23 (FGF23) which, in turn, requires the membrane protein Klotho as a coreceptor [8][9][10].…”
Background/Aims: Epidemiological evidence suggests that vitamin D deficiency is associated with anemia. The potent metabolite 1,25(OH)2 vitamin D3 [1,25(OH)2D3] activates various signaling cascades regulating a myriad of cellular functions including suicidal cell death or apoptosis. Suicidal death of erythrocytes or eryptosis is characterized by cell shrinkage and cell membrane scrambling leading to phosphatidylserine (PS) externalization. Stimulation of eryptosis may limit lifespan of circulating erythrocytes and thus cause anemia. In the present study, we explored the effect of a high vitamin D diet (10,000 I.U. vitamin D for 14 days) in mice on eryptosis. Methods: Plasma concentrations of erythropoietin were estimated using an immunoassay kit, blood count using an electronic hematology particle counter, relative reticulocyte numbers using Retic-COUNT® reagent, PS exposure at the cell surface from annexin V binding, cell volume from forward scatter, and cytosolic Ca2+ ([Ca2+]i) from Fluo3-fluorescence in FACS analysis. Results: Vitamin D treatment decreased mean corpuscular volume, reticulocyte count, and plasma erythropoietin levels. Vitamin D treatment slightly but significantly decreased forward scatter but did not significantly modify spontaneous PS exposure and [Ca2+]i of freshly drawn erythrocytes. Vitamin D treatment augmented the stimulation of PS exposure and cell shrinkage following exposure to hyperosmotic shock (addition of 550 mM sucrose) or energy depletion (glucose removal) without significantly modifying [Ca2+]i. Conclusions: The present observations point to a subtle effect of exogenous vitamin D supplementation on erythrocyte survival.
“…A previous study [87] also highlighted the ability of 1,25(OH)2D3 to inhibit the maturation of plasma cells and class-switched memory B cells, suggesting a potential role for vitamin D in B-cell-related disorders such as SLE. Notably, 1,25(OH)2D3, inhibits NF-kB pathway and p105/p50 protein expression of human naïve B cells, by impairing nuclear translocation of p65 and consequently reducing binding of p65 to its binding site in the p105 promoter.…”
Section: Vitamin D Dietary Supplementationmentioning
SLE-related risk factors involve both disease- and treatment-related features, including disease activity, disease phenotype, corticosteroid misuse and alterations of innate and adaptive immunity. Primary prevention is mandatory in management of lupus patients through appropriate disease control, corticosteroid tapering, use of antimalarials and eventually vitamin D supplementation.
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