Induction of monocytic differentiation and bone resorption by 1,25-dihydroxyvitamin D3.

Bar‐Shavit, Zvi; Teitelbaum, Steven L.; Reitsma, Pieter H.; Hall, A.K.; Pegg, Lyle E.; Trial, JoAnn; Kahn, Arnold J.

doi:10.1073/pnas.80.19.5907

Cited by 362 publications

(157 citation statements)

References 25 publications

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“…The effective concentration range of calcitriol for FBPase induction is approximately consistent with those for the inductions of lysozyme in HL-60 [21] and M-I [22] cells, of alkaline phosphatase in ROS17/2 cells [23] and of nitroblue-tetrazolium-reducing capability in U937 cells [24]. The induced enzyme activity is strongly inhibited by AMP, a specific allosteric inhibitor of FBPase, and precipitated with anti-(rat liver FBPase) serum.…”

Section: Discussionmentioning

confidence: 75%

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Induction and Turnover of Fructose 1,6‐Bisphosphatase in HL‐60 Leukemia Cells by Calcitriol

Mizunuma

Tashima

1994

European Journal of Biochemistry

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Fructose 1,6-bisphosphatase mRNA and enzyme activity in HL-60 cells were rapidly and markedly induced by calcitriol (formerly known as la,25-dihydroxyvitamin D3). The activity reached 70-80 times the basal level after 96 h. The enzyme activity in the cells incubated for 96 h with calcitriol decreased immediately after its withdrawal but after a 24-h incubation the activity in the cells continued to increase slightly and then decreased slowly. Calcitriol increased the enzyme activity dose-dependently with maximal stimulation at 10 nM and half-maximal at 2.1 nM. The rate of synthesis of fructose 1,6-bisphosphatase almost paralleled the increase in inRNA level during treatment with calcitriol. When calcitriol was removed from media after incubation for either 24 h or 96 h, fructose-1;6-bisphosphatase mRNA and fructose-l,6-bisphosphatase synthesis decreased rapidly to the basal level. The enzyme was only slightly degraded in the cells incubated with calcitriol for 24 h followed by the subsequent culture without calcitriol but it was degraded with a half-life estimated to be approximately 64 h in the same cells followed by culturing with calcitriol. In the cells incubated for 96 h, the same degradation rate (i.e. half-life =64 h) was observed irrespective of the following culture with or without calcitriol. Calcitriol did not affect the degradation rate of total soluble proteins.Fructose 1,6-bisphosphatase (FBPase) is one of the ratelimiting enzymes in hepatic gluconeogenesis. The in vivo level of FBPase is under nutritional and hormonal controls. The intracellular concentration of the enzyme in the liver increases under gluconeogenic conditions including fasting, a high-protein diet and alloxan diabetes [l]. The enzyme concentration is also increased by the injection of glucagon, glucocorticoids and thyroxine [2]. El-Maghrabi et al. showed that FBPase mRNA was increased in livers from adult diabetic rats and was reduced to control levels after insulin treatment [3]. Recently, they observed the accumulation of FBPase mRNA in primary hepatocyte cultures incubated with cAMP and showed the presence of CAMP-responsive elements in the 5'-flanking region of the rat FBPase gene [4].FBPase is present in fetal liver and increases exponentially during fetal development [ 5 ] . In organ culture from fetal mouse liver, the activity of FBPase is remarkably elevated in the presence of dibutyryl cAMP [6, 71. FBPase activity, however, increases during the culture even in the absence of an inducer, although at lower rates [6]. The increase in intracellular FBPase concentration, especially in fetal development, might also be regulated by another factor (s) in addition to elevation of CAMP.

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Section: Discussionmentioning

confidence: 75%

“…HL-60 cells are induced to differentiate into monocytemacrophages by calcitriol [21,26,271. Like calcitriol, 12-O-tetradecanoyl-phorbol 13-acetate also induces HL-60 cells into monocyte-macrophage differentiation [28 -301.…”

Section: Discussionmentioning

confidence: 99%

Induction and Turnover of Fructose 1,6‐Bisphosphatase in HL‐60 Leukemia Cells by Calcitriol

Mizunuma

Tashima

1994

European Journal of Biochemistry

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“…There is substantial evidence that it induces differentiation in cells of the mononuclear phagocyte series, including such osteoclast characteristics as multinuclearity, carbonic anhydrase II expression and vitronectin receptors (Abe et al 1983, Bar-Shavit et al 1983, Billecocq et al 1990, Medhora et al 1993. Induction of lacunar bone resorption, however, depends on contact with osteoblastic or bone marrow stromal cells, which also express 1,25(OH) 2 D 3 receptors, and it is not known whether 1,25(OH) 2 D 3 induces osteoclast formation through actions on stromal cells, osteoclastic precursors, or both (Chambers 1992).…”

Section: Introductionmentioning

confidence: 99%

Induction of osteoclast formation by parathyroid hormone depends on an action on stromal cells

Fuller

Owens²,

Chambers³

1998

Journal of Endocrinology

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It is believed that parathyroid hormone (PTH) increases the resorptive activity of pre-existing osteoclasts through a primary interaction with cells of the osteoblastic lineage. Much less is known, however, of the mechanisms by which PTH induces osteoclast formation. It is known that osteoclast formation occurs through a contact-dependent interaction between stromal cells and haemopoietic precursors, but it is not known whether PTH acts on stromal cells or precursors to induce osteoclast formation. To address this issue, we compared the ability of haemopoietic cultures to generate osteoclasts, identified as calcitonin receptor positive (CTRP) cells, and to resorb bone in response to PTH and 1,25(OH) 2 vitamin D 3 (1,25(OH) 2 D 3 ). We found that when murine haemopoietic tissues were incubated at densities sufficiently high to support haemopoiesis, both PTH and 1,25(OH) 2 D 3 induced bone resorption in bone marrow cells, but in cultures of haemopoietic spleen only 1,25(OH) 2 D 3 induced CTRP cells, and neither hormone induced bone resorption. To determine whether these differences were attributable to differences in stromal cells or haemopoietic precursors, lower densities of haemopoietic spleen cells were incubated on osteoblastic (UMR 106), splenic or bone marrow stromal cells. We found that the behaviour of the cocultures reflected the characteristics and origin of the stromal cells. Thus, the ability of both osteoblastic and splenic stromal cells to induce CTRP cells with 1,25(OH) 2 D 3 , while only osteoblastic cells induced osteoclasts with PTH, from the same precursors, suggests that the ability of PTH to induce osteoclastic differentiation cannot be attributed to a hormonal action on osteoclast precursors, but depends on a response in stromal cells.

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“…The active form of 1,25(OH) 2 D 3 and its analogues have been reported to inhibit cell growth and induce differentiation in both normal and malignant cell types. [38][39][40][41][42] The results of the current study demonstrated a numerical reduction of tumor volume in CAC-8-bearing mice treated with 1,25(OH) 2 D 3 and its analogues (EB1089 and analog V). CAC-8-bearing mice treated with analog V maintained body weight better than other CAC-8-bearing groups.…”

Section: Discussionmentioning

confidence: 96%

Effects of 1,25-Dihydroxyvitamin D3 [1,25(OH)2D3] and Its Analogues (EB1089 and Analog V) on Canine Adenocarcinoma (CAC-8) in Nude Mice

Kunakornsawat

Rosol

Capen

et al. 2002

Biological & Pharmaceutical Bulletin

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Recently the active form of vitamin D, 1a,25-dihydroxyvitamin D 3 , [1,25(OH) 2 D 3 ] and its synthetic analogues have been shown to exert anti-tumor effects both in vitro and in vivo. [1][2][3][4][5] As summarized by Johannes et al.,6) many investigations have reported that 1,25(OH) 2 D 3 and its analogues affect tumor cells due to: a) blockade of the cells in the G 1 /G 0 phase and reduction of the number of cells in S phase of cell cycle progression, 7-9) b) induction of apoptosis, 10,11) c) expression and regulation of oncogenes and tumor suppressor genes, [12][13][14] d) interaction with tumor-or stroma-derived growth factors for growth inhibition [e.g. transforming growth factor (TGFb), insulin-like growth factor (IGF)], [15][16][17] and e) induction of differentiation. 18,19) However, most studies have been completed in human tumors with little information available in other species on the effects of 1,25(OH) 2 D 3 and its analogues.This study examined the effects of 1,25(OH) 2 D 3 and its analogues [22,24-diene-24a,26a,27a-trihomo-1a ,25-dihydroxyvitamin D 3 (EB1089) and 1,25-dihydroxy-16-ene-23-yne-vitamin D 3 (analog V)] on the canine adenocarcinoma (CAC-8) model of humoral hypercalcemia of malignancy (HHM) in nude mice. Canine adenocarcinoma derived from apocrine glands of the anal sac is commonly associated with cancer-associated hypercalcemia. [20][21][22] HHM is a paraneoplastic syndrome in dogs that significantly contributes to the morbidity and mortality of cancer patients. It is well documented that an autonomous overproduction of parathyroid hormone-related protein (PTHrP) is the principal humoral factor that causes hypercalcemia in dogs with this carcinoma due to increased release of calcium from bone and enhanced reabsorption of calcium in the kidney. 22,23) The inhibitory effect of 1,25(OH) 2 D 3 and its analogues on PTHrP production thus far has been reported on both normal human cells 24,25) and human tumor cells. [26][27][28][29][30] In order to achieve the inhibitory effect of 1,25(OH) 2 D 3 on PTHrP production, high doses and/or prolonged treatment with this potent active vitamin D metabolite most likely will be needed, which has the potential to enhance the hypercalcemia. 1,25(OH) 2 D 3 itself is also an important regulator of bone development, bone metabolism, calcium homeostasis and increases blood calcium. 31) In order to minimize this potential toxic effect, vitamin D analogues have been synthesized with noncalcemic effect. Among these noncalcemic analogues, EB1089 and analog V, have been studied on tumor growth.1,2,32) The effects of these two analogues (EB1089 and analog V) on canine adenocarcinoma model of HHM in nude mice were evaluated in this study. The specific objectives were to determine the effects of 1,25(OH) 2 D 3 and its analogues on tumor growth and body weight, changes in plasma ionized calcium, PTHrP production, bone resorption, and the distribution of the 1,25(OH) 2 D 3 receptor (VDR) on tumors in CAC-8-bearing mice. * To whom correspondence should be addressed...

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Induction of monocytic differentiation and bone resorption by 1,25-dihydroxyvitamin D3.

Cited by 362 publications

References 25 publications

Induction and Turnover of Fructose 1,6‐Bisphosphatase in HL‐60 Leukemia Cells by Calcitriol

Induction and Turnover of Fructose 1,6‐Bisphosphatase in HL‐60 Leukemia Cells by Calcitriol

Induction of osteoclast formation by parathyroid hormone depends on an action on stromal cells

Effects of 1,25-Dihydroxyvitamin D<sub>3</sub> [1,25(OH)<sub>2</sub>D<sub>3</sub>] and Its Analogues (EB1089 and Analog V) on Canine Adenocarcinoma (CAC-8) in Nude Mice

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