Rapid publication: Constitutive expression of a vitamin D 1-hydroxylase in a myelomonocytic cell line: A model for studying 1,25-dihydroxyvitamin D production in vitro

Adams, John S.; Beeker, Timothy G.; Hongo, Takashi; Clemens, Thomas L.

doi:10.1002/jbmr.5650051212

Cited by 32 publications

(20 citation statements)

References 23 publications

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“…We confirmed that human osteoclasts, derived from human PBMC, possess the molecular machinery to both metabolise and respond to 25D, since they express cytoplasmic CYP27B1 and nuclear VDR proteins. The latter observation is consistent with cells of the monocyte/macrophage lineage being a well-characterized site of extra-renal synthesis of 1,25D [10,11]. We also used the RAW 264.7 cell model to confirm that, in our hands, these cells could synthesise detectable 1,25D from exogenous 25D (data not shown), consistent with a previous report [12].…”

Section: Discussionsupporting

confidence: 91%

“…The intriguing possibility exists that osteoclasts also participate in local production of, as well as response to, 1,25D. Indeed, cells of the monocyte/macrophage lineage are known to express CYP27B1 and convert 25D into 1,25D [10,11]. The RAW 264.7 cell line has been shown to express CYP27B1 mRNA, levels of which increased during their differentiation into osteoclast-like cells [12].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The metabolism of 25-(OH)vitamin D3 by osteoclasts and their precursors regulates the differentiation of osteoclasts

Kogawa

Anderson

Findlay

et al. 2010

The Journal of Steroid Biochemistry and Molecular Biology

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

The metabolism of 25-(OH)vitamin D3 by osteoclasts and their precursors regulates the differentiation of osteoclasts

Kogawa

Anderson

Findlay

et al. 2010

The Journal of Steroid Biochemistry and Molecular Biology

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“…As mentioned previously, cells of the monocyte/macrophage lineage have been shown to express CYP27B1 and convert 25D into 1,25D (Adams et al, 1990;Dusso et al, 1991). Bone marrow macrophages have also been found to convert 25D into either 1,25D or 24,25D.…”

Section: Bone Cells As Sources Of 125dmentioning

confidence: 91%

“…These include the skin Lehmann and Meurer (2003), Schuessler et al (2001), Bikle (2004) and the liver (Hollis, 1990), and a variety of haemopoietic cells and tissues, including lymph nodes (Zehnder et al, 2001), activated monocytes/macrophages (Adams et al, 1990;Dusso et al, 1991) and dendritic cells (Hewison et al, 2003). Except in cases of certain tumour derived 1,25D (Anderson et al, 2004), extrarenal production does not appear to contribute significantly to circulating levels.…”

Section: Bone Cells As Sources Of 125dmentioning

confidence: 99%

The skeleton as an intracrine organ for vitamin D metabolism

Anderson

Atkins

2008

Molecular Aspects of Medicine

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“…These data suggest that 25(OH)D 3 metabolism in cells of the osteoclast lineage optimizes osteoclastogenesis and regulates the resorptive behavior of mature osteoclasts. Cells of the monocyte/macrophage lineage have been shown to express Cyp27b1 mRNA and convert 25(OH)D 3 into 1,25(OH) 2 D 3 [40,41]. Bone marrow macrophages also convert 25(OH)D 3 into either 1,25 (OH) 2 D 3 or 24,25(OH) 2 D 3 .…”

Section: Exogenous and Endogenous Sources Of 125(oh) 2 Dmentioning

confidence: 99%

Target Genes

et al. 2011

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Genome-wide analyses indicate vitamin D, through its active metabolite 1,25-dihydroxyvitamin D 3 (1,25 (OH) 2 D 3 ) and the vitamin D receptor (VDR), has a potential to regulate the expression of some 3000 genes [1]. However, current evidence indicates that the strongest phenotype exhibited by vitamin-D-deficient humans or animals relates to impaired skeletal health. The first scientific reports in the early 1900s that rickets was due to vitamin D 3 deficiency placed vitamin D as central to the regulation of calcium and phosphate homeostasis. In this context, it appears that the most critical and most widely studied endocrine role of vitamin D is its contribution to the maintenance of plasma calcium and phosphate at physiological levels through regulation of intestinal absorption of dietary calcium and phosphate.A central question, however, is whether vitamin D acts directly on bone tissue to modulate bone mineral homeostasis and bone strength. This question has been difficult to answer conclusively due in part to the direct actions of vitamin D on plasma calcium and phosphate levels, which indirectly affect bone mineralization and structure. One direct action that has been clearly demonstrated is the ability of plasma 1,25(OH) 2 D 3 , at least at supraphysiological levels, to stimulate bone resorption by the activation of osteoclasts [2].The effects of vitamin D deficiency on bone in vivo can apparently be largely corrected by increasing dietary calcium and phosphate [3,4], suggesting that vitamin D is not an absolute requirement for optimal bone health. Indeed, the fact that the osteomalacic phenotype observed in the vitamin D receptor gene knockout (Vdr KO ) mouse can be rescued by feeding a diet containing high levels of calcium and phosphate has led some to conclude that VDR-mediated activity in bone is essentially redundant [5,6]. Others have suggested that actions of VDR in bone may in fact impair mineralization [7,8]. These conclusions are, however, difficult to reconcile against an accumulating large body of evidence indicating that vitamin D activity in bone is critical for bone cell differentiation and optimal mineral status [9e12]. In this chapter, we examine the evidence for direct effects of vitamin D on the bone as a tissue, and its actions on the constituent cells of bone, in particular bone-matrix-forming osteoblasts, osteocytes, and bone-resorbing osteoclasts.There is now evidence that each of the major bone cells is capable of producing 1,25(OH) 2 D 3 from the 25-hydroxyvitamin D 3 (25(OH)D 3 ) precursor, and that this activity is likely to account for the skeletal effects of circulating 25(OH)D 3 (see Fig. 23.1). On the weight of this evidence, we have proposed that bone is an intracrine organ of vitamin D metabolism [13]. The actions of 1,25(OH) 2 D 3 are mediated ultimately by direct effects on individual vitamin-D-responsive genes. However, the effects of vitamin D on bone tissue as a whole are not yet fully understood but are likely due to a combination of direct effects via VDREs, downstr...

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Rapid publication: Constitutive expression of a vitamin D 1-hydroxylase in a myelomonocytic cell line: A model for studying 1,25-dihydroxyvitamin D production in vitro

Cited by 32 publications

References 23 publications

The metabolism of 25-(OH)vitamin D3 by osteoclasts and their precursors regulates the differentiation of osteoclasts

The metabolism of 25-(OH)vitamin D3 by osteoclasts and their precursors regulates the differentiation of osteoclasts

The skeleton as an intracrine organ for vitamin D metabolism

Target Genes

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