Contrasting effects of 1,25-dihydroxyvitamin D3 on bone matrix and mineral appositional rates in the mouse

Marie, Pierre J.; Hott, M.; Garba, Marie-Thérèse

doi:10.1016/0026-0495(85)90030-7

Cited by 40 publications

(16 citation statements)

References 16 publications

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“…It is well established that calcitriol directly stimulates in vitro bone formation (35) and mineralized matrix formation by osteoblasts (36). This effect was recently confirmed in transgenic mice overexpressing the vitamin D receptor, which featured increased cortical bone thickness and mineral density (37).…”

Section: Discussionmentioning

confidence: 78%

Targeted deletion of histidine decarboxylase gene in mice increases bone formation and protects against ovariectomy-induced bone loss

Fitzpatrick

Buzás

Gagne

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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Targeted disruption of the histidine decarboxylase gene (HDC ؊/؊ ), the only histamine-synthesizing enzyme, led to a histamine-deficient mice characterized by undetectable tissue histamine levels, impaired gastric acid secretion, impaired passive cutaneous anaphylaxis, and decreased mast cell degranulation. We used this model to study the role of histamine in bone physiology. Compared with WT mice, HDC ؊/؊ mice receiving a histamine-free diet had increased bone mineral density, increased cortical bone thickness, higher rate of bone formation, and a marked decrease in osteoclasts. After ovariectomy, cortical and trabecular bone loss was reduced by 50% in HDC ؊/؊ mice compared with WT. Histamine deficiency protected the skeleton from osteoporosis directly, by inhibiting osteoclastogenesis, and indirectly, by increasing calcitriol synthesis. Quantitative RT-PCR showed elevated 25-hydroxyvitamin D-1␣-hydroxylase and markedly decreased 25-hydroxyvitamin D-24-hydroxylase mRNA levels. Serum parameters confirming this indirect effect included elevated calcitriol, phosphorus, alkaline phosphatase, and receptor activator of NF-B ligand concentrations, and suppressed parathyroid hormone concentrations in HDC ؊/؊ mice compared with WT mice. After ovariectomy, histamine-deficient mice were protected from bone loss by the combination of increased bone formation and reduced bone resorption.

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Section: Discussionmentioning

confidence: 78%

Targeted deletion of histidine decarboxylase gene in mice increases bone formation and protects against ovariectomy-induced bone loss

Fitzpatrick

Buzás

Gagne

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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“…Conflicting results have been re ported in the rat since the chronic administration of calci triol or 1 -alpha-vitamin D j has been observed to decrease the osteoclast surface or number in some studies [27,30,31 ] and to increase the osteoclast surface or number in others [26,28,29], Holtrop et al [16] have reported that calcitriol stimu lates osteoclast activity in the parathyroidectomized rat; however, this observation was primarily based on changes in osteoclast morphology during a 48-hour period after a single, high dose of calcitriol. Mailuche et al [19] studied the effect of chronic calcitriol supplementation in para thyroidectomized dogs and did not observe any increase in the number of osteoclasts, but did report an increase in bone resorption per osteoclast in calcitriol-supplemented dogs.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have been performed in animals to evaluate the effect of calcitriol on bone [26][27][28][29][30][31], The prob lem with most of these studies is that it is difficult to sepa rate the interaction between calcitriol and PTH from a direct effect of calcitriol; moreover, with one exception [19], these studies have been performed in animals with normal renal function. Conflicting results have been re ported in the rat since the chronic administration of calci triol or 1 -alpha-vitamin D j has been observed to decrease the osteoclast surface or number in some studies [27,30,31 ] and to increase the osteoclast surface or number in others [26,28,29], Holtrop et al [16] have reported that calcitriol stimu lates osteoclast activity in the parathyroidectomized rat; however, this observation was primarily based on changes in osteoclast morphology during a 48-hour period after a single, high dose of calcitriol.…”

Section: Discussionmentioning

confidence: 99%

Studies in a Hemodialysis Patient Indicating that Calcitriol May Have a Direct Suppressive Effect on Bone

Pahl¹,

Jara²,

Bover³

et al. 1995

Nephron

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Calcitriol putatively suppresses bone activity by decreasing parathyroid hormone (PTH) levels. Results of studies in a 52-year-old female maintenance hemodialysis patient suggest that calcitriol may also have a direct suppressive effect on bone. The PTH-calcium relationship was evaluated through the use of low (1 mEq/1) and high (4 mEq/1) calcium hemodialyses that were performed before the initiation of calcitriol treatment, at the end of 6 weeks of thrice-weekly intravenous calcitriol administration, and 6 weeks after the discontinuation of calcitriol. During the low-calcium dialysis, serum calcium decreased more rapidly and to a greater magnitude after calcitriol treatment despite no appreciable difference in basal and maximally stimulated PTH levels; during the high-calcium dialysis, calcitriol treatment resulted in a more rapid increase in serum calcium despite no appreciable difference in basal and maximally suppressed PTH levels. Discontinuation of calcitriol resulted in responses to the low and high calcium dialyses that were similar to those observed before calcitriol treatment. In conclusion, the results suggest that calcitriol may have a direct suppressive effect on bone that is independent of PTH.

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“…For routine histologic analysis, the caudal vertebrae and bones of the hindlimbs were fixed in formalin, decalcified in 10% Na2EDTA (pH 6.9) and stained with hematoxylin and eosin. For histomorphometric analysis, mice received intraperitoneal injections of tetracycline as described (14). After necropsy, bone tissue was fixed in formalin, dehydrated in acetone, embedded in methylacrylate, sectioned, stained by the modified Masson method, and histomorphometrically analyzed (15 (19)], washed, and autoradiographed (11).…”

mentioning

confidence: 99%

Osteoporosis induced in mice by overproduction of interleukin 4.

Lewis

Liggitt

Effmann

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

141

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Osteoporosis is a common disease in which loss of bone mass results in skeletal fragility. The development of therapies for this disorder has been hampered by the lack of a convenient animal model. Here we describe a disorder in bone homeostasis in transgenic mice that inappropriately express the cytokine interleukin 4 (IL-4) under the direction of the lymphocyte-specific proximal promoter for the kck gene. Bone disease in Ick-IL-4 mice appeared to result from markedly decreased bone formation by osteoblasts, features strikingly similar to those observed in cases ofsevere low-turnover human involutional osteoporosis. By 2 months of age, female and male Ick-IL-4 mice invariably developed severe osteoporosis of both cortical and trabecular bone. Osteoporosis was observed in two independently derived founder animals, indicating that this phenotype was directly mediated by the IL-4 transgene.

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Contrasting effects of 1,25-dihydroxyvitamin D3 on bone matrix and mineral appositional rates in the mouse

Cited by 40 publications

References 16 publications

Targeted deletion of histidine decarboxylase gene in mice increases bone formation and protects against ovariectomy-induced bone loss

Targeted deletion of histidine decarboxylase gene in mice increases bone formation and protects against ovariectomy-induced bone loss

Studies in a Hemodialysis Patient Indicating that Calcitriol May Have a Direct Suppressive Effect on Bone

Osteoporosis induced in mice by overproduction of interleukin 4.

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