The vitamin D receptor, the skin and stem cells

@article{Luderer2010TheVD,
  title={The vitamin D receptor, the skin and stem cells},
  author={Hilary F Luderer and Marie B. Demay},
  journal={The Journal of Steroid Biochemistry and Molecular Biology},
  year={2010},
  volume={121},
  pages={314-316}
}
  • Hilary F LudererM. Demay
  • Published 1 July 2010
  • Biology, Medicine
  • The Journal of Steroid Biochemistry and Molecular Biology

The Impact of Vitamin D on Skin Aging

Active forms of vitamin D3 including its canonical (1,25(OH)2D3) and noncanonical (CYP11A1-intitated) D3 derivatives as well as L3 derivatives are promising agents for the prevention, attenuation, or treatment of premature skin aging.

The role of vitamin D receptor mutations in the development of alopecia

The role of vitamin D3 and vitamin B9 (Folic acid) in immune system

These findings provide a new link between diet and the immune system, which could maintain the immunological homeostasis and clarify the beneficial roles of vitamins in informing the design of vitamin analogs as pharmacologic agents for the generation and maintenance of a healthy immune condition.

Skeletal and Extraskeletal Actions of Vitamin D: Current Evidence and Outstanding Questions

There is a need for continued ongoing and future basic and clinical studies to better define whether vitamin D status can be optimized to improve many aspects of human health, and what is plausible regarding the health effects of vitamin D.

The renaissance of vitamin D.

The role of vitamin D as a global regulator of homeostasis from a historical perspective, its relevance to human physiology and pathology and existence of alternative pathways ofitamin D metabolism and multiple intracellular targets broadens the understanding of its physiological activities.

Mutations in the vitamin D receptor and hereditary vitamin D-resistant rickets.

Heterogeneous loss of function mutations in the vitamin D receptor (VDR) interfere with vitamin D signaling and cause hereditary vitamin D-resistant rickets (HVDRR). HVDRR is characterized by

Enhanced Differentiation of Stromal Cells and Embryonic Stem Cells with Vitamin D3

Results with E14 and OP9 cells indicate that adequate VD3 concentration enhances cellular differentiation and inhibits proliferation, and suggest that if E14/OP9 cells were co-cultured andVD3-treated, there would be further-enhanced differentiation of ESCs into blood cells.

Enhanced Differentiation of Stromal Cells and Embryonic Stem Cells with Vitamin D 3 E World

The results indicate that adequate VD3 concentration enhances cellular differentiation and inhibits proliferation, and suggest that if E14 and OP9 cells were co-cultured andVD3-treated, there would be furtherenhanced differentiation of ESCs into blood cells.

Functional Analysis of VDR Gene Mutation R343H in A Child with Vitamin D-Resistant Rickets with Alopecia

To determine the VDR mutation and the mechanisms of this mutation-causing phenotype in a family with HVDRR and alopecia, a novel homozygous missense R343H mutation in the exon 9 of VDR residing in the retinoid X receptor (RXR)-binding domain was identified.

References

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Ligand-independent actions of the vitamin D receptor maintain hair follicle homeostasis.

It is demonstrated that the effects of the VDR on the hair follicle are ligand independent and point to novel molecular and cellular actions of this nuclear receptor.

Vitamin D receptor is essential for normal keratinocyte stem cell function

Absence of the VDR impairs canonical Wnt signaling in keratinocytes and leads to the development of alopecia due to a defect inkeratinocyte stem cells, as demonstrated by transient gene expression assays.

Evaluation of keratinocyte proliferation and differentiation in vitamin D receptor knockout mice.

The data suggest that the alopecia in the VDR null mice is not attributable to an intrinsic defect in keratinocyte proliferation or differentiation, but rather to an abnormality in initiation of the hair cycle.

Targeting expression of the human vitamin D receptor to the keratinocytes of vitamin D receptor null mice prevents alopecia.

Although these studies demonstrate that expression of the VDR in keratinocytes is necessary, they do not prove that it is sufficient for maintenance of the normal hair cycle, and restoration of VDR expression in the keratinocyte of V DR null mice, prevents the hair cycle defect that leads to the development of alopecia.

Vitamin D and human health: lessons from vitamin D receptor null mice.

The precise mode of action and the full spectrum of activities of the vitamin D hormone, 1,25-dihydroxyvitamin D [1,25-(OH)(2)D], can now be better evaluated by critical analysis of mice with engineered deletion of the Vitamin D receptor (VDR).

Metabolic and cellular analysis of alopecia in vitamin D receptor knockout mice.

Alopecia in the VDR-null mice is due to a defect in epithelial-mesenchymal communication that is required for normal hair cycling, and the keratinocyte is identified as the cell of origin of the defect.

Vitamin D, calcium, and epidermal differentiation.

I. Introduction THE SKIN is the sole source of cholecalciferol or vitamin D3 (D3), the precursor for a family of vitamin D metabolites whose best understood role is the regulation of bone mineral

Deletion of deoxyribonucleic acid binding domain of the vitamin D receptor abrogates genomic and nongenomic functions of vitamin D.

It is shown that gene-targeted mutant mice express a VDR with an intact hormone binding domain, but lacking the first zinc finger necessary for DNA binding, supporting the conclusion that the classical VDR mediates the nongenomic actions of 1,25-(OH)(2)D(3).

Mice lacking the vitamin D receptor exhibit impaired bone formation, uterine hypoplasia and growth retardation after weaning

It is reported here that in VDR null mutant mice, no defects in development and growth were observed before weaning, irrespective of reduced expression of vitamin D target genes, which establishes a critical role for VDR in growth, bone formation and female reproduction in the post-weaning stage.

Targeted ablation of the vitamin D receptor: an animal model of vitamin D-dependent rickets type II with alopecia.

  • Y. LiA. Pirro M. Demay
  • Medicine, Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 1997
A mouse model of VDDR II is generated by targeted ablation of the second zinc finger of the VDR DNA-binding domain and homozygous mice are phenotypically normal at birth and demonstrate normal survival at least until 6 months, compared to animals made vitamin D deficient by dietary means.