Narrow-band UVB effects on cutaneous vitamin D receptor expression and serum 25-hydroxyvitamin D in generalized vitiligo

2017 ◽  
Vol 34 (3) ◽  
pp. 175-183 ◽  
Author(s):  
Hala M. El-hanbuli ◽  
Noha M. Dawoud ◽  
Rania H. Mahmoud
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Narrow Band ◽  
Receptor Expression ◽  
Hydroxyvitamin D ◽  
25 Hydroxyvitamin D

scholarly journals Coronary artery vitamin D receptor expression and plasma concentrations of 25-hydroxyvitamin D

2012 ◽  
Vol 19 (9) ◽  
pp. 967-973 ◽  
Author(s):  
Peter F. Schnatz ◽  
Matthew Nudy ◽  
David M. O’Sullivan ◽  
Xuezhi Jiang ◽  
J. Mark Cline ◽  
...  
Keyword(s):  
Vitamin D ◽  
Coronary Artery ◽  
Vitamin D Receptor ◽  
Plasma Concentrations ◽  
Receptor Expression ◽  
Hydroxyvitamin D ◽  
25 Hydroxyvitamin D

scholarly journals Vitamin D-Mediated Hypercalcemia: Mechanisms, Diagnosis, and Treatment

2016 ◽  
Vol 37 (5) ◽  
pp. 521-547 ◽  
Author(s):  
Peter J. Tebben ◽  
Ravinder J. Singh ◽  
Rajiv Kumar
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Active Form ◽  
Elevated Serum ◽  
Diagnosis And Treatment ◽  
Vitamin D Metabolites ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
Stone Formers ◽  
25 Hydroxyvitamin D

AbstractHypercalcemia occurs in up to 4% of the population in association with malignancy, primary hyperparathyroidism, ingestion of excessive calcium and/or vitamin D, ectopic production of 1,25-dihydroxyvitamin D [1,25(OH)2D], and impaired degradation of 1,25(OH)2D. The ingestion of excessive amounts of vitamin D3 (or vitamin D2) results in hypercalcemia and hypercalciuria due to the formation of supraphysiological amounts of 25-hydroxyvitamin D [25(OH)D] that bind to the vitamin D receptor, albeit with lower affinity than the active form of the vitamin, 1,25(OH)2D, and the formation of 5,6-trans 25(OH)D, which binds to the vitamin D receptor more tightly than 25(OH)D. In patients with granulomatous disease such as sarcoidosis or tuberculosis and tumors such as lymphomas, hypercalcemia occurs as a result of the activity of ectopic 25(OH)D-1-hydroxylase (CYP27B1) expressed in macrophages or tumor cells and the formation of excessive amounts of 1,25(OH)2D. Recent work has identified a novel cause of non-PTH-mediated hypercalcemia that occurs when the degradation of 1,25(OH)2D is impaired as a result of mutations of the 1,25(OH)2D-24-hydroxylase cytochrome P450 (CYP24A1). Patients with biallelic and, in some instances, monoallelic mutations of the CYP24A1 gene have elevated serum calcium concentrations associated with elevated serum 1,25(OH)2D, suppressed PTH concentrations, hypercalciuria, nephrocalcinosis, nephrolithiasis, and on occasion, reduced bone density. Of interest, first-time calcium renal stone formers have elevated 1,25(OH)2D and evidence of impaired 24-hydroxylase-mediated 1,25(OH)2D degradation. We will describe the biochemical processes associated with the synthesis and degradation of various vitamin D metabolites, the clinical features of the vitamin D-mediated hypercalcemia, their biochemical diagnosis, and treatment.

scholarly journals Tumor Autonomous Effects of Vitamin D Deficiency Promote Breast Cancer Metastasis

Endocrinology ◽  
2016 ◽  
Vol 157 (4) ◽  
pp. 1341-1347 ◽  
Author(s):  
Jasmaine D. Williams ◽  
Abhishek Aggarwal ◽  
Srilatha Swami ◽  
Aruna V. Krishnan ◽  
Lijuan Ji ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Cancer Metastasis ◽  
Receptor Expression ◽  
Inverse Association ◽  
Primary Tumors ◽  
Hydroxyvitamin D ◽  
25 Hydroxyvitamin D ◽  
Vitamin D Signaling

Abstract Patients with breast cancer (BCa) frequently have preexisting vitamin D deficiency (low serum 25-hydroxyvitamin D) when their cancer develops. A number of epidemiological studies show an inverse association between BCa risk and vitamin D status in humans, although some studies have failed to find an association. In addition, several studies have reported that BCa patients with vitamin D deficiency have a more aggressive molecular phenotype and worse prognostic indicators. However, it is unknown whether this association is mechanistically causative and, if so, whether it results from systemic or tumor autonomous effects of vitamin D signaling. We found that ablation of vitamin D receptor expression within BCa cells accelerates primary tumor growth and enables the development of metastases, demonstrating a tumor autonomous effect of vitamin D signaling to suppress BCa metastases. We show that vitamin D signaling inhibits the expression of the tumor progression gene Id1, and this pathway is abrogated in vitamin D deficiency in vivo in 2 murine models of BCa. These findings are relevant to humans, because we discovered that the mechanism of VDR regulation of Inhibitor of differentiation 1 (ID1) is conserved in human BCa cells, and there is a negative correlation between serum 25-hydroxyvitamin D levels and the level of ID1 in primary tumors from patients with BCa.

scholarly journals Role of the vitamin D receptor in FGF23 action on phosphate metabolism

2005 ◽  
Vol 390 (1) ◽  
pp. 325-331 ◽  
Author(s):  
Yoshio Inoue ◽  
Hiroko Segawa ◽  
Ichiro Kaneko ◽  
Setsuko Yamanaka ◽  
Kenichiro Kusano ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Fibroblast Growth Factor 23 ◽  
Mrna Levels ◽  
Dna Encoding ◽  
Vitamin D Metabolism ◽  
Hydroxyvitamin D ◽  
Naked Dna ◽  
25 Hydroxyvitamin D

FGF23 (fibroblast growth factor 23) is a novel phosphaturic factor that influences vitamin D metabolism and renal re-absorption of Pi. The goal of the present study was to characterize the role of the VDR (vitamin D receptor) in FGF23 action using VDR(−/−) (VDR null) mice. Injection of FGF23M (naked DNA encoding the R179Q mutant of human FGF23) into VDR(−/−) and wildtype VDR(+/+) mice resulted in an elevation in serum FGF23 levels, but had no effect on serum calcium or parathyroid hormone levels. In contrast, injection of FGF23M resulted in significant decreases in serum Pi levels, renal Na/Pi co-transport activity and type II transporter protein levels in both groups when compared with controls injected with mock vector or with FGFWT (naked DNA encoding wild-type human FGF23). Injection of FGF23M resulted in a decrease in 25-hydroxyvitamin D 1α-hydroxylase mRNA levels in VDR(−/−) and VDR(+/+) mice, while 25-hydroxyvitamin D 24-hydroxylase mRNA levels were significantly increased in FGF23M-treated animals compared with mock vector control- or FGF23WT-treated animals. The degree of 24-hydroxylase induction by FGF23M was dependent on the VDR, since FGF23M significantly reduced the levels of serum 1,25(OH)2D3 [1,25-hydroxyvitamin D3] in VDR(+/+) mice, but not in VDR(−/−) mice. We conclude that FGF23 reduces renal Pi transport and 25-hydroxyvitamin D 1α-hydroxylase levels by a mechanism that is independent of the VDR. In contrast, the induction of 25-hydroxyvitamin D 24-hydroxylase and the reduction of serum 1,25(OH)2D3 levels induced by FGF23 are dependent on the VDR.

scholarly journals Vitamin D receptor ChIP-seq in primary CD4+ cells: relationship to serum 25-hydroxyvitamin D levels and autoimmune disease

BMC Medicine ◽  
2013 ◽  
Vol 11 (1) ◽  
Author(s):  
Adam E Handel ◽  
Geir K Sandve ◽  
Giulio Disanto ◽  
Antonio J Berlanga-Taylor ◽  
Giuseppe Gallone ◽  
...  
Keyword(s):  
Vitamin D ◽  
Autoimmune Disease ◽  
Vitamin D Receptor ◽  
Cd4 Cells ◽  
Hydroxyvitamin D ◽  
25 Hydroxyvitamin D
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