ArticleEndocrinology2020
The Vitamin D Receptor in Osteoblast-Lineage Cells Is Essential for the Proresorptive Activity of 1α,25(OH)2D3 In Vivo.
Article in Endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 43 citations in OpenAlex.
- Bone transcriptomics reveals that juzentaihoto remodels and activates multiple pathways in Klotho-deficient mice.Bone reports · 2026Article
- FXR in bone metabolism: An emerging regulator.iScience · 2026Review
- Vitamin D Receptor Signaling and Ligand Modulation: Molecular Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2026Review
- The role of fat-soluble vitamins on bone metabolism and osteoporosis: a literature review.Annals of medicine · 2025Review
- Does higher serum 25-hydroxyvitamin D levels will harm bone mineral density?: a cross-sectional study.BMC endocrine disorders · 2024Article
- Coactivator-independent vitamin D receptor signaling causes severe rickets in mice, that is not prevented by a diet high in calcium, phosphate, and lactose.Bone research · 2024Article
- Efficacy of denosumab in the treatment of hypercalcemic renal dysfunction in sarcoidosis: a case report.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2024Article
- The complex relationship between vitamin D and kidney stones: balance, risks, and prevention strategies.Frontiers in nutrition · 2024Review
- Vitamins as regulators of calcium-containing kidney stones - new perspectives on the role of the gut microbiome.Nature reviews. Urology · 2023Review
- The role of prostate-specific antigen in the osteoblastic bone metastasis of prostate cancer: a literature review.Frontiers in oncology · 2023Review
- Effects of vitamin D with or without calcium on pathological ossification: A retrospective clinical study.Experimental and therapeutic medicine · 2022Article
- 1,25-D3 attenuates cerebral ischemia injury by regulating mitochondrial metabolismFrontiers in aging neuroscience · 2022Article
- 1α,25-Dihydroxyvitamin D3 Promotes Angiogenesis After Cerebral Ischemia Injury in Rats by Upregulating the TGF-β/Smad2/3 Signaling Pathway.Frontiers in cardiovascular medicine · 2022Article
- Galectin-3 Contributes to the Inhibitory Effect of lα,25-(OH)International journal of molecular sciences · 2021Article
- Integrated View on the Role of Vitamin D Actions on Bone and Growth Plate Homeostasis.JBMR plus · 2021Article
- Calcitriol confers neuroprotective effects in traumatic brain injury by activating Nrf2 signaling through an autophagy-mediated mechanism.Molecular medicine (Cambridge, Mass.) · 2021Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported that daily administration of a pharmacological dose of eldecalcitol, an analog of 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3], increased bone mass by suppressing bone resorption. These antiresorptive effects were found to be mediated by the vitamin D receptor (VDR) in osteoblast-lineage cells. Using osteoblast-lineage-specific VDR conditional knockout (Ob-VDR-cKO) mice, we examined whether proresorptive activity induced by the high-dose 1α,25(OH)2D3 was also mediated by VDR in osteoblast-lineage cells. Administration of 1α,25(OH)2D3 (5 μg/kg body weight/day) to wild-type mice for 4 days increased the number of osteoclasts in bone and serum concentrations of C-terminal crosslinked telopeptide of type I collagen (CTX-I, a bone resorption marker). The stimulation of bone resorption was concomitant with the increase in serum calcium (Ca) and fibroblast growth factor 23 (FGF23) levels, and decrease in body weight. This suggests that a toxic dose of 1α,25(OH)2D3 can induce bone resorption and hypercalcemia. In contrast, pretreatment of wild-type mice with neutralizing anti-receptor activator of NF-κB ligand (RANKL) antibody inhibited the 1α,25(OH)2D3-induced increase of osteoclast numbers in bone, and increase of CTX-I, Ca, and FGF23 levels in serum. The pretreatment with anti-RANKL antibody also inhibited the 1α,25(OH)2D3-induced decrease in body weight. Consistent with observations in mice conditioned with anti-RANKL antibody, the high-dose administration of 1α,25(OH)2D3 to Ob-VDR-cKO mice failed to significantly increase bone osteoclast numbers, serum CTX-I, Ca, or FGF23 levels, and failed to reduce the body weight. Taken together, this study demonstrated that the proresorptive, hypercalcemic, and toxic actions of high-dose 1α,25(OH)2D3 are mediated by VDR in osteoblast-lineage cells.
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