Markers Indicating Body Vitamin D Stores and Responses of Liver and Adipose Tissues to Changes in Vitamin D Intake in Male Mice

Kiourtzidis, Mikis; Kühn, Julia; Brandsch, Corinna; Baur, Anja-Christina; Wensch-Dorendorf, Monika; Stangl, Gabriele I.

doi:10.3390/nu12051391

Cited by 7 publications

(3 citation statements)

References 31 publications

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“…Vitamin D was dissolved in PBS buffer and 0.25 ug/kg/d administered to mice by intragastrical administration as previously reported. 31 In addition, 1,25VD was dissolved in absolute ethyl alcohol, to achieve different concentrations of 1,25VD at 4 μM, 20 μM and 100 μM which were used to treat cells for 48h. PMA was dissolved in dimethyl sulfoxide to achieve a concentration of 1μM which was used to treat cells.…”

Section: Methodsmentioning

confidence: 99%

1,25-Dihydroxyvitamin D Inhibits Osteoarthritis by Modulating Interaction Between Vitamin D Receptor and NLRP3 in Macrophages

Duan¹,

Ma²,

W³

et al. 2021

JIR

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Background Osteoarthritis (OA) is the most prevalent chronic joint disease globally. Loss of extracellular matrix (ECM) by chondrocytes is a classic feature of OA. Inflammatory cytokines, such as interleukin-1β (IL-1β) and interleukin-18 (IL-18), secreted mainly by macrophages, promote expression of matrix degrading proteins and further aggravate progression of OA. 1,25-dihydroxyvitamin D (1,25VD) modulates inflammation thus exerting protective effects on cartilage tissue. However, the underlying mechanisms of 1,25VD activity have not been fully elucidated. Methods The destabilization of the medial meniscus (DMM)-induced mice model of OA was established to investigate the protective effects of 1,25VD by micro-CT and Safranin-O and Fast Green staining. And the co-culture system between THP-1 cells and primary chondrocytes was constructed to explore the effects of vitamin D receptor (VDR) and 1,25VD on chondrogenic proliferation, apoptosis, and migration. The immunofluorescence staining and Western blot analysis were used to detect the expressions of ECM proteins and matrix degradation-associated proteases. Enzyme-linked immunosorbent assay (ELISA) was used to examine the expression levels of inflammatory cytokines. Results The findings of the study showed that 1,25VD prevented cartilage degeneration and osteophyte formation by inhibiting secretion of inflammatory cytokines in OA mice model. These protective effects were exerted through the vitamin D receptor (VDR). Further studies showed that 1,25VD increased ubiquitination level of NLRP3 by binding to VDR, resulting in decrease in IL-1β and IL-18 secretion. These findings indicate that 1,25VD binds to VDR thus preventing chondrogenic ECM degradation by modulating macrophage NLRP3 activation and secretion of inflammatory cytokines, thus alleviating OA progression. Conclusion Here, our study suggests that 1,25VD, targeting to VDR, prevents chondrogenic ECM degradation through regulating macrophage NLRP3 activation and inflammatory cytokines secretion, thereby alleviating OA. These findings provide information on a novel molecular mechanism for application of 1,25VD as OA therapy.

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Section: Methodsmentioning

confidence: 99%

1,25-Dihydroxyvitamin D Inhibits Osteoarthritis by Modulating Interaction Between Vitamin D Receptor and NLRP3 in Macrophages

Duan¹,

Ma²,

W³

et al. 2021

JIR

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“…Both skin-synthesized vitamin D 3 and food/supplement-derived D 2/3 are catalyzed by 25-hydroxylase [mainly cytochrome P450 family 27 subfamily A member 1 (CYP27A1) and cytochrome P450 family 2 subfamily R member 1 (CYP2R1)] to 25(OH)D in the liver. Due to its long half-life [13] and strong vitamin D binding protein (VDBP) binding ability [14], serum 25(OH)D is the most abundant and stable vitamin D metabolite in the circulation; hence, its serum concentration is used to evaluate the nutritional status of vitamin D [15]. Subsequently, 25(OH)D is catalyzed by 25(OH)D-1α hydroxylase, cytochrome P450 family 27 subfamily B member 1 (CYP27B1), to 1,25(OH) 2 D in the kidney, which can bind to the VDR in the target tissue and regulate physiological processes.…”

Section: Introductionmentioning

confidence: 99%

Exercise: A Possibly Effective Way to Improve Vitamin D Nutritional Status

Zhang

Cao

2022

Nutrients

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Vitamin D deficiency has become a widespread public health problem owing to its potential adverse health effects. Generally, the nutritional status of vitamin D depends on sunlight exposure and dietary or supplementary intake. However, recent studies have found that exercise can influence circulating 25(OH)D levels; although, the results have been inconclusive. In this review, we focused on the effect of exercise on circulating vitamin D metabolites and their possible mechanisms. We found that endurance exercise can significantly increase serum 25(OH)D levels in vitamin D-deficient people but has no significant effect on vitamin D-sufficient people. This benefit has not been observed with resistance training. Only chronic endurance exercise training can significantly increase serum 1,25(OH)2D, and the effect may be sex-dependent. Exercise may influence 25(OH)D levels in the circulation by regulating either the vitamin D metabolites stored in tissues or the utilization by target tissues. The effects of exercise on 25(OH)D levels in the circulation may be dependent on many factors, such as the vitamin D nutritional status, exercise type and intensity, and sex. Therefore, further research on the effects and mechanisms of exercise on vitamin D metabolites is required.

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“…Phorbol myristate acetate (PMA), LPS And Nigericin (Nig) were purchased from Sigma-Aldrich (P1585, 916374 and N7143, respectively). Vitamin D was dissolved in PBS buffer and 0.25 ug/kg/d administered to mice by intragastrical administration as previously reported [31]. In addition, 1,25 VD was dissolved in absolute ethyl alcohol, to achieve different concentrations of 1,25 VD at 4 µM, 20 µM and 100 µM which were used to treat cells.…”

Section: Administration Of Drugsmentioning

confidence: 99%

1,25-dihydroxyvitamin D Inhibits Osteoarthritis by Modulating Interaction Between Vitamin D Receptor and NLRP3 in Macrophages

Duan

Liu

et al. 2021

Preprint

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Background: Osteoarthritis (OA) is most prevalent chronic joint disease globally. Loss of extracellular matrix (ECM) by chondrocytes is a classical feature of OA. Inflammatory cytokines, such as interleukin-1β (IL-1β) and interleukin-18 (IL-18), secreted mainly by macrophages, promote expression of matrix degrading proteins and further aggravate progression of OA. 1,25-dihydroxyvitamin D (1,25 VD) modulating inflammation thus exerting protective effects on cartilage tissue. However, the underlying mechanisms of 1,25 VD activity have not been fully elucidated.Design: The destabilization of the medial meniscus (DMM)-induced mice model of OA was established to investigate the protective effects of 1,25 VD by micro-CT and Safranin-O and Fast Green staining. And the co-culture system between THP-1 cells and primary chondrocytes was constructed to explore the effects of vitamin D receptor (VDR) and 1,25 VD on chondrogenic proliferation, apoptosis, and migration. The immunofluorescence staining and western blot analysis were used to detect the expressions of ECM proteins and matrix degradation associated proteases. Enzyme-linked immunosorbent assay (ELISA) was used to examine the expression levels of inflammatory cytokines.Results: The findings of the study showed that 1,25 VD prevented cartilage degeneration and osteophyte formation by inhibiting secretion of inflammatory cytokines in OA mice model. These protective effects were exerted through the vitamin D receptor (VDR). Further studies showed that 1,25VD increased ubiquitination level of NLRP3 by binding to VDR, resulting in decrease in IL-1β and IL-18 secretion. These findings indicate that 1,25 VD binds to VDR thus preventing chondrogenic ECM degradation by modulating macrophage NLRP3 activation and secretion of inflammatory cytokines, thus alleviating OA progression.Conclusions: Here, our study suggests that 1,25 VD, targeting to VDR, prevents chondrogenic ECM degradation through regulating macrophage NLRP3 activation and inflammatory cytokines secretion, thereby alleviates OA. These findings provide information on a novel molecular mechanism for application of 1,25 VD as OA therapy.

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Markers Indicating Body Vitamin D Stores and Responses of Liver and Adipose Tissues to Changes in Vitamin D Intake in Male Mice

Cited by 7 publications

References 31 publications

1,25-Dihydroxyvitamin D Inhibits Osteoarthritis by Modulating Interaction Between Vitamin D Receptor and NLRP3 in Macrophages

1,25-Dihydroxyvitamin D Inhibits Osteoarthritis by Modulating Interaction Between Vitamin D Receptor and NLRP3 in Macrophages

Exercise: A Possibly Effective Way to Improve Vitamin D Nutritional Status

1,25-dihydroxyvitamin D Inhibits Osteoarthritis by Modulating Interaction Between Vitamin D Receptor and NLRP3 in Macrophages

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