Correlation of enhanced cell proliferation with decreased density of vitamin D receptor in parathyroid hyperplasia in chronic dialysis patients

Nephrology ◽  
1997 ◽  
Vol 3 (3) ◽  
pp. 279-284 ◽  
Author(s):  
Taro KOIKE ◽  
Naoko FUKUDA ◽  
Masafumi FUKAGAWA ◽  
Kazuo OHTA ◽  
Kiyoshi KUROKAWA
Keyword(s):  
Vitamin D ◽  
Cell Proliferation ◽  
Vitamin D Receptor ◽  
Parathyroid Hyperplasia ◽  
Chronic Dialysis ◽  
Dialysis Patients

Lipid profiles and vitamin D receptor polymorphisms in overweight/obese dialysis patients

2017 ◽  
Author(s):  
Gokhan Bagci ◽  
Can Huzmeli ◽  
Binnur Bagci ◽  
Ferhan Candan ◽  
Lale Akkaya ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Lipid Profiles ◽  
Dialysis Patients

scholarly journals Stimulation of Sirt1-Regulated FoxO Protein Function by the Ligand-Bound Vitamin D Receptor

2010 ◽  
Vol 30 (20) ◽  
pp. 4890-4900 ◽  
Author(s):  
Beum-Soo An ◽  
Luz E. Tavera-Mendoza ◽  
Vassil Dimitrov ◽  
Xiaofeng Wang ◽  
Mario R. Calderon ◽  
...  
Keyword(s):  
Vitamin D ◽  
Cell Proliferation ◽  
Phosphatase Activity ◽  
Vitamin D Receptor ◽  
Nuclear Export ◽  
Target Genes ◽  
Trichostatin A ◽  
Control Cell ◽  
Sirtuin 1 ◽  
Foxo Protein

ABSTRACT Hormonal vitamin D, 1,25-dihydroxyvitamin D (1,25D), signals through the nuclear vitamin D receptor (VDR). 1,25D regulates cell proliferation and differentiation and has been identified as a cancer chemopreventive agent. FoxO proteins are transcription factors that control cell proliferation and survival. They function as tumor suppressors and are associated with longevity in several organisms. Accumulating data have revealed that 1,25D and FoxO proteins regulate similarly common target genes. We show here that the ligand-bound VDR regulates the posttranslational modification and function of FoxO proteins. 1,25D treatment enhances binding of FoxO3a and FoxO4 within 4 h to promoters of FoxO target genes and blocks mitogen-induced FoxO protein nuclear export. The VDR associates directly with FoxO proteins and regulators, the sirtuin 1 (Sirt1) class III histone deacetylase (HDAC), and protein phosphatase 1. In addition, phosphatase activity and trichostatin A-resistant HDAC activity coimmunoprecipitate with the VDR. 1,25D treatment rapidly (in <4 h) induces FoxO deacetylation and dephosphorylation, consistent with activation. In contrast, ablation of VDR expression enhances FoxO3a phosphorylation, as does knockdown of Sirt1, consistent with the coupling of FoxO acetylation and phosphorylation. 1,25D regulation of common VDR/FoxO target genes is attenuated by blockade of phosphatase activity or by small interfering RNA (siRNA)-mediated knockdown of Sirt1 or FoxO protein expression. Finally, 1,25D-dependent cell cycle arrest is blocked in FoxO3a-deficient cells, indicating that FoxO proteins are key downstream mediators of the antiproliferative actions of 1,25D. These studies link 1,25D signaling through the VDR directly to Sirt1 and FoxO function and provide a molecular basis for the cancer chemopreventive actions of 1,25D.

scholarly journals Serum vitamin D levels are positively associated with varicella zoster immunity in chronic dialysis patients

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Chia-Ter Chao ◽  
Szu-Ying Lee ◽  
Wei-Shun Yang ◽  
Chung-Jen Yen ◽  
Chih-Kang Chiang ◽  
...  
Keyword(s):  
Vitamin D ◽  
Serum Vitamin ◽  
Chronic Dialysis ◽  
Dialysis Patients ◽  
Varicella Zoster ◽  
Serum Vitamin D ◽  
Vitamin D Levels

Pharmacodynamic Effects of Sucroferric Oxyhydroxide and Sevelamer Carbonate on Vitamin D Receptor Agonist Bioactivity in Dialysis Patients

2016 ◽  
Vol 44 (2) ◽  
pp. 104-112 ◽  
Author(s):  
Stuart M. Sprague ◽  
Adrian C. Covic ◽  
Jürgen Floege ◽  
Markus Ketteler ◽  
Jaco Botha ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Phosphate Binders ◽  
Similar Degree ◽  
Dialysis Patients ◽  
Treatment Groups ◽  
Pharmacodynamic Effects ◽  
Sevelamer Carbonate ◽  
Post Hoc ◽  
Potential Interactions

Background: Many patients with chronic kidney disease are prescribed vitamin D receptor agonists (VDRAs) for the management of secondary hyperparathyroidism. Oral phosphate binders may interact with, and potentially reduce the therapeutic activity of, oral VDRAs. This post hoc analysis of a Phase 3 study evaluated the pharmacodynamic effects of the iron-based phosphate binder sucroferric oxyhydroxide (SFOH) and sevelamer (SEV) carbonate on VDRA activity in dialysis patients. Methods: One thousand and fifty nine patients were randomized to SFOH 1.0-3.0 g/day (n = 710) or SEV 2.4-14.4 g/day (n = 349) for up to 52 weeks. Potential interactions of SFOH and SEV with VDRAs were assessed using serum intact parathyroid hormone (iPTH) concentrations as a pharmacodynamic biomarker. Three populations of SFOH- and SEV-treated patients were analyzed: Population 1 (n = 187), patients taking concomitant stable doses of oral VDRAs only; Population 2 (n = 250), patients taking no concomitant VDRAs; Population 3 (n = 68), patients taking concomitant stable doses of intravenous paricalcitol only. Populations were compared using a mixed-effects model to obtain the least squares mean change in iPTH from baseline to Week 52. Differences between treatment groups were also compared. Results: In Population 1, iPTH decreased from baseline to Week 52 in the SFOH group (-25.3 pg/ml) but increased in the SEV group (89.8 pg/ml) (p = 0.02). In Population 2, iPTH increased to a similar extent in both treatment groups. In Population 3, iPTH concentrations in both treatment groups decreased to a similar degree (-29.6 and -11.4 pg/ml for SFOH and SEV, respectively; p = 0.87). Conclusions: In contrast with SEV, SFOH did not appear to impact the iPTH-lowering effect of oral VDRAs.

scholarly journals Possible prevention of uremic nausea by vitamin D receptor activators in non-dialysis patients with stage 5 chronic kidney disease

2016 ◽  
Vol 21 (5) ◽  
pp. 825-834
Author(s):  
Masato Ikeda ◽  
Yoshimi Ueda ◽  
Yukio Maruyama ◽  
Keitaro Yokoyama ◽  
Takashi Yokoo ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Vitamin D Receptor ◽  
Dialysis Patients

scholarly journals 1,25(OH)2Vitamin D3 Stimulates Myogenic Differentiation by Inhibiting Cell Proliferation and Modulating the Expression of Promyogenic Growth Factors and Myostatin in C2C12 Skeletal Muscle Cells

Endocrinology ◽  
2011 ◽  
Vol 152 (8) ◽  
pp. 2976-2986 ◽  
Author(s):  
Leah A. Garcia ◽  
Keisha K. King ◽  
Monica G. Ferrini ◽  
Keith C. Norris ◽  
Jorge N. Artaza
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Cell Proliferation ◽  
Vitamin D Receptor ◽  
Myogenic Differentiation ◽  
Receptor Expression ◽  
Negative Regulator ◽  
Muscle Performance ◽  
Rt Pcr ◽  
C2c12 Myoblasts

Skeletal muscle wasting is an important public health problem associated with aging, chronic disease, cancer, kidney dialysis, and HIV/AIDS. 1,25-Dihydroxyvitamin D (1,25-D3), the active form of vitamin D, is widely recognized for its regulation of calcium and phosphate homeostasis in relation to bone development and maintenance and for its calcemic effects on target organs, such as intestine, kidney, and parathyroid glands. Emerging evidence has shown that vitamin D administration improves muscle performance and reduces falls in vitamin D-deficient older adults. However, little is known of the underlying mechanism or the role 1,25-D3 plays in promoting myogenic differentiation at the cellular and/or molecular level. In this study, we examined the effect of 1,25-D3 on myoblast cell proliferation, progression, and differentiation into myotubes. C2C12 myoblasts were treated with 1,25-D3 or placebo for 1, 3, 4, 7, and 10 d. Vitamin D receptor expression was analyzed by quantitative RT-PCR, Western blottings and immunofluorescence. Expression of muscle lineage, pro- and antimyogenic, and proliferation markers was assessed by immunocytochemistry, PCR arrays, quantitative RT-PCR, and Western blottings. Addition of 1,25-D3 to C2C12 myoblasts 1) increased expression and nuclear translocation of the vitamin D receptor, 2) decreased cell proliferation, 3) decreased IGF-I expression, and 4) promoted myogenic differentiation by increasing IGF-II and follistatin expression and decreasing the expression of myostatin, the only known negative regulator of muscle mass, without changing growth differentiation factor 11 expression. This study identifies key vitamin D-related molecular pathways for muscle regulation and supports the rationale for vitamin D intervention studies in select muscle disorder conditions.

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