Vitamin D receptor agonists’ anti‐inflammatory properties

Vojinović, Jelena

doi:10.1111/nyas.12429

Cited by 48 publications

(28 citation statements)

References 84 publications

(144 reference statements)

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“…An experimental study in which rats with hepatic steatosis received cholecalciferol reported improved cognitive effects and reduced TNF-a levels in brain [33]. Therefore, the observed benefits may have resulted from the anti-inflammatory properties of vitamin D [34], a finding that supports the inflammatory hypothesis for some types of depression.…”

Section: Discussionmentioning

confidence: 81%

Vitamin D supplementation reduces depressive symptoms in patients with chronic liver disease

et al. 2016

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Section: Discussionmentioning

confidence: 81%

Vitamin D supplementation reduces depressive symptoms in patients with chronic liver disease

et al. 2016

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“…Recently, vitamin D is recognized for its non-classical actions including the modulation of innate immune and the regulation of cell proliferation1920. Indeed, vitamin D is a potent anti-inflammatory agent212223. Vitamin D itself is devoid of biological activity.…”

mentioning

confidence: 99%

Vitamin D3 inhibits lipopolysaccharide-induced placental inflammation through reinforcing interaction between vitamin D receptor and nuclear factor kappa B p65 subunit

Chen¹,

et al. 2015

Sci Rep

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It is increasingly recognized that vitamin D3 (VitD3) has an anti-inflammatory activity. The present study investigated the effects of maternal VitD3 supplementation during pregnancy on LPS-induced placental inflammation and fetal intrauterine growth restriction (IUGR). All pregnant mice except controls were intraperitoneally injected with LPS (100 μg/kg) daily from gestational day (GD)15–17. In VitD3 + LPS group, pregnant mice were orally administered with VitD3 (25 μg/kg) before LPS injection. As expected, maternal LPS exposure caused placental inflammation and fetal IUGR. Interestingly, pretreatment with VitD3 repressed placental inflammation and protected against LPS-induced fetal IUGR. Further analysis showed that pretreatment with VitD3, which activated placental vitamin D receptor (VDR) signaling, specifically suppressed LPS-induced activation of nuclear factor kappa B (NF-κB) and significantly blocked nuclear translocation of NF-κB p65 subunit in trophoblast gaint cells of the labyrinth layer. Conversely, LPS, which activated placental NF-κB signaling, suppressed placental VDR activation and its target gene expression. Moreover, VitD3 reinforced physical interaction between placental VDR and NF-κB p65 subunit. The further study demonstrates that VitD3 inhibits placental NF-κB signaling in VDR-dependent manner. These results provide a mechanistic explanation for VitD3-mediated anti-inflammatory activity. Overall, the present study provides evidence for roles of VDR as a key regulator of placental inflammation.

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“…Besides the mineral metabolism, it has anti-inflammatory effects [4, 5]. Studies of cultured cells and animal models have shown that 1,25D 3 attenuates the effects of LPS.…”

Section: Introductionmentioning

confidence: 99%

1,25-Dihydroxyvitamin D3 Attenuates the Effects of Lipopolysaccharide by Causing ADAM10-Dependent Ectodomain Shedding of Toll-Like Receptor 4

Yang

Kim

Han

et al. 2017

Cell Physiol Biochem

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Background/Aims: We investigated how 1,25-dihydroxyvitamin D₃ (1,25D₃) inhibits the effects of lipopolysaccharide (LPS) in human aortic endothelial cells. Methods: Cellular signaling was explored by determination of protein abundance with Western blot, measurement of cytosolic Ca²⁺ concentration and immunofluorescence staining for a disintegrin and metalloprotease 10 (ADAM10). Results: LPS stimulated the expression of intercellular adhesion molecule 1 (ICAM-1) through toll-like receptor 4 (TLR4) and subsequent activation of p38 mitogen-activated protein kinase (p38 MAPK). Pretreatment with 1,25D₃ attenuated LPS-induced p38 MAPK activation and ICAM-1 expression by causing ectodomain shedding of TLR4. This effect of 1,25D₃ depended on its ability to induce a rapid extracellular Ca²⁺ influx through L-type calcium channels because the ectodomain shedding was prevented by the absence of extracellular Ca²⁺ or the presence of verapamil. TLR4 ectodomain shedding was also induced by Bay K8644 (L-type calcium channel agonist). Both 1,25D₃ and Bay K8644 caused extracellular Ca²⁺ influx-dependent ADAM10 translocation to the cell surface. Depletion of ADAM10 by siRNA transfection prevented 1,25D₃- and Bay K8644-induced ectodomain shedding of TLR4, and abolished the inhibitory effect of 1,25D₃ on LPS-induced ICAM-1 expression. Conclusion: 1,25D₃ causes ectodomain shedding of TLR4 and thereby decreases the responsiveness of cells to LPS. ADAM10, activated by extracellular Ca²⁺ influx, was implicated in the ectodomain cleavage of TLR4.

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Vitamin D receptor agonists’ anti‐inflammatory properties

Cited by 48 publications

References 84 publications

Vitamin D supplementation reduces depressive symptoms in patients with chronic liver disease

Vitamin D supplementation reduces depressive symptoms in patients with chronic liver disease

Vitamin D3 inhibits lipopolysaccharide-induced placental inflammation through reinforcing interaction between vitamin D receptor and nuclear factor kappa B p65 subunit

1,25-Dihydroxyvitamin D3 Attenuates the Effects of Lipopolysaccharide by Causing ADAM10-Dependent Ectodomain Shedding of Toll-Like Receptor 4

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