The vitamin D receptor functions as a transcription regulator in the absence of 1,25-dihydroxyvitamin D3
Open accessAbstract
The vitamin D receptor (VDR) is a critical mediator of the biological actions of 1,25-dihydroxyvitamin D 3 (1,25(OH)2 D 3). As a nuclear receptor, ligand activation of the VDR leads to the protein's binding to specific sites on the genome that results in the modulation of target gene expression. The VDR is also known to play a role in the hair cycle, an action that appears to be 1,25(OH)2 D 3-independent. Indeed, in the absence of the VDR as in hereditary 1,25-dihydroxyvitamin D resistant rickets (HVDRR) both skin defects and alopecia emerge. Recently, we generated a mouse model of HVDRR without alopecia wherein a mutant human VDR lacking 1,25(OH)2 D 3-binding activity was expressed in the absence of endogenous mouse VDR. While 1,25(OH)2 D 3 failed to induce gene expression in these mice, resulting in an extensive skeletal phenotype, the receptor was capable of restoring normal hair cycling. We also noted a level of secondary hyperparathyroidism that was much higher than that seen in the VDR null mouse and was associated with an exaggerated bone phenotype as well. This suggested that the VDR might play a role in parathyroid hormone (PTH) regulation independent of 1,25(OH)2 D 3. To evaluate this hypothesis further, we contrasted PTH levels in the HVDRR mouse model with those seen in Cyp27b1 null mice where the VDR was present but the hormone was absent. The data revealed that PTH was indeed higher in Cyp27b1 null mice compared to VDR null mice. To evaluate the mechanism of action underlying such a hypothesis, we measured the expression levels of a number of VDR target genes in the duodena of wildtype mice and in transgenic mice expressing either normal or hormone-binding deficient mutant VDRs. We also compared expression levels of these genes between VDR null mice and Cyp27b1 null mice. In a subset of cases, the expression of VDR target genes was lower in mice containing the VDR as opposed to mice that did not. We suggest that the VDR may function as a selective suppressor/de-repressor of gene expression in the absence of 1,25(OH)2 D 3.
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- Authors
- Lee, S. M., & Pike, J. W.
- Affiliations
- University of Wisconsin–Madison (US)
- Corresponding author
- Lee, Seong Min
- Venue
- The Journal of Steroid Biochemistry and Molecular Biology
- Publisher
- Elsevier BV
- Published
- 2016-11
- Volume
- 164
- Pages
- 265-270
- ISSN
- 0960-0760 (ISSN-L)
- PMC
- PMC4769962
- OpenAlex
- W1569138725
- Cited by
- 39
- References
- 40
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 3 · 2023: 7 · 2022: 3 · 2021: 2 · 2020: 3 · 2019: 3 · 2018: 4 · 2017: 7 · 2016: 2 · 2015: 1
- FWCI
- 3.70
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Steroid Biochemistry and Molecular Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK072281, R01DK073995)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR045173)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Vitamin D Research Studies
- Health Sciences › Medicine › Urology › Hair Growth and Disorders
- Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
- Keywords
- vitamin D receptor, 1,25-dihydroxyvitamin D3, hereditary vitamin D-resistant rickets, hair cycle, hair loss, secondary hyperparathyroidism, parathyroid hormone, CYP27B1, gene expression regulation, nuclear receptors, duodenum, skeletal phenotype, transgenic mouse model, derepression
- MeSH terms
- Animals, Bone and Bones, Calcitriol, Disease Models, Animal, Gene Expression Regulation, Hair, Humans, Parathyroid Hormone, Transcription, Genetic, 25-Hydroxyvitamin D3 1-alpha-Hydroxylase, Signal Transduction, Receptors, Calcitriol, Mice, Knockout, Mice, Rickets, Hypophosphatemic
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