Metabolism of vitamin D3 in human osteoblasts: Evidence for autocrine and paracrine activities of 1α,25-dihydroxyvitamin D3

Atkins, Gerald J.; Anderson, Paul; Findlay, David M.; Welldon, Katie J.; Vincent, C.; Zannettino, Andrew C.W.; O’Loughlin, Peter; Morris, Howard A.

doi:10.1016/j.bone.2007.02.024

Cited by 224 publications

(228 citation statements)

References 53 publications

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“…Strong support for the importance of intracellularly produced over circulating 1,25-(OH) 2 D 3 in regulating cellular functions comes from the elegant study of Rowling et al (2006), who have shown that in mammary gland cells, VDR-mediated actions depended more on megalin-mediated endocytosis of 25-(OH)D 3 than on ambient 1,25-(OH) 2 D 3 . Likewise, van Driel et al (2006) and Atkins et al (2007) showed that human osteoblasts express megalin and, when treated with 25-(OH)D 3 , produce sufficient 1,25-(OH) 2 D 3 to induce typical expression of osteocalcin, osteopontin and RANKL (receptor activator for nuclear factor k B ligand). In addition, Lechner et al (2007) could induce the characteristic anti-mitogenic effect of 1,25-(OH) 2 D 3 when 25-(OH)D-1a-hydroxylase positive human colon carcinoma cells were treated with 25-(OH)D 3 .…”

Section: Vitamin D and Calcium Actions: Molecular And Cellular Aspectsmentioning

confidence: 99%

“…This process is tightly controlled by VDR-mediated effects of 1,25-(OH) 2 D 3 on temporal expression of genes coding for the non-collagenous matrix proteins, which are necessary for initiation of the mineralization process (Owen et al, 1991). Osteoblasts are an important source of 1,25-(OH) 2 D 3 , because they exhibit 25-(OH)D-1a-hydroxylase activity (Atkins et al, 2007). In vitamin D deficiency, however, a lack of endogenously produced 1,25-(OH) 2 D 3 may retard osteoblast differentiation and, therefore, also mineralization of the organic matrix.…”

Section: Vitamin D and Calcium Actions And Interactions: Pathophysiolmentioning

confidence: 99%

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Vitamin D and calcium insufficiency-related chronic diseases: molecular and cellular pathophysiology

Peterlik¹,

Cross²

2009

Eur J Clin Nutr

101

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A compromised vitamin D status, characterized by low 25-hydroxyvitamin D (25-(OH)D) serum levels, and a nutritional calcium deficit are widely encountered in European and North American countries, independent of age or gender. Both conditions are linked to the pathogenesis of many degenerative, malignant, inflammatory and metabolic diseases. Studies on tissue-specific expression and activity of vitamin D metabolizing enzymes, 25-(OH)D-1a-hydroxylase and 25-(OH)D-24-hydroxylase, and of the extracellular calcium-sensing receptor (CaR) have led to the understanding of how, in non-renal tissues and cellular systems, locally produced 1,25-dihydroxyvitamin D 3 (1,25-(OH) 2 D 3 ) and extracellular Ca 2 þ act jointly as key regulators of cellular proliferation, differentiation and function. Impairment of cooperative signalling from the 1,25-(OH) 2 D 3 -activated vitamin D receptor (VDR) and from the CaR in vitamin D and calcium insufficiency causes cellular dysfunction in many organs and biological systems, and, therefore, increases the risk of diseases, particularly of osteoporosis, colorectal and breast cancer, inflammatory bowel disease, insulin-dependent diabetes mellitus type I, metabolic syndrome, diabetes mellitus type II, hypertension and cardiovascular disease. Understanding the underlying molecular and cellular processes provides a rationale for advocating adequate intake of vitamin D and calcium in all populations, thereby preventing many chronic diseases worldwide.

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Section: Vitamin D and Calcium Actions: Molecular And Cellular Aspectsmentioning

confidence: 99%

Section: Vitamin D and Calcium Actions And Interactions: Pathophysiolmentioning

confidence: 99%

Vitamin D and calcium insufficiency-related chronic diseases: molecular and cellular pathophysiology

Peterlik¹,

Cross²

2009

Eur J Clin Nutr

101

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“…The mouse MC3T3-E1 (ATCC CRL-2593) and the human osteosarcoma SaOS-2 cells lines (ATCC HTB-85) were used (Wang et al, 1999;Atkins et al, 2007). Cells were plated on glass cover slips for immunofl uorescence analysis (24-well plates, 20,000 cells/well) and directly on plastic for mineralisation assays (6-well plates, 60,000 cells/well) and maintained in α-minimal essential medium (alpha-MEM) (Invitrogen, Burlington, ON, Canada) with 10 % foetal bovine serum (FBS), 50 μg/mL ascorbic acid (Sigma-Aldrich, Oakville, Ontario, Canada) and 10 mM β-glycerophosphate (Sigma-Aldrich), and medium changed every 3 days.…”

Section: Cell Culture Studies Mc3t3-e1 and Saos-2 Cellsmentioning

confidence: 99%

Ameloblastin is not implicated in bone remodelling and repair

Kuroda

Wazen²,

Sellin³

et al. 2011

eCM

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Ameloblastin (AMBN) is an enamel matrix protein produced by ameloblasts. It has been suggested that AMBN might also be implicated in craniofacial bone formation. Our objective was to determine whether AMBN has an effect on osteogenic mineralisation and infl uences bone remodelling and repair. MC3T3-E1 cells were screened for endogenous expression of enamel proteins using real time PCR. Various osteogenic cells were infected with lentivirus encoding for AMBN and protein expression was verifi ed using immunochemistry. Cultures were stained with alizarin red and mineralisation was quantifi ed. Healing bone was probed for expression of AMBN by DNA microarray analysis. Tooth extraction, experimental tooth movement (ETM), and creation of a non-critical size bone defect in the tibia (BDT) were carried out in wild type and AMBN Δ5-6 mutant mice. Tissues were processed for immunolabelling of AMBN and Bril, an osteoblast specifi c protein associated with active bone formation. MC3T3-E1 cells and healing bone showed no significant expression of AMBN. Overexpression of AMBN in osteogenic cultures induced no noticeable changes in mineralisation. In wild type mice, AMBN was immunodetected in ameloblasts and enamel, but not in normal bone, and at sites where bone remodelling and repair were induced. Bone remodelling during ETM and BDT repair in AMBN Δ5-6 mice were not signifi cantly different from that in wild type animals. Our results suggest that AMBN does not infl uence osteogenic activity in vitro under the conditions used, and does not participate in craniofacial bone remodelling under mechanical stress and in repair of non-critical size bone defects.

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“…A resposta dos osteoblastos à VitD pode variar, dependendo do estágio de diferenciação dessas células: células imaturas respondem a partir de uma ação osteoclástica evidenciada pela expressão de RANKL; nas células maduras, a resposta é osteogênica (6) . Já existem elementos suficientes que demonstram que tanto as respostas osteogênicas quanto as osteoclastogênicas por osteoblastos podem ser reguladas por níveis de VitD circulantes in vivo (5) .…”

Section: Discussionunclassified

“…Como demonstrado, níveis adequados de VitD e seu metabolismo são importantes em vários aspectos para a saúde óssea do esqueleto, tendo em vista que já foi comprovado que a 25D otimiza tanto a diferenciação osteoblástica quanto a mineralização óssea (5) . Assim, estudos experimentais in vivo com diferentes níveis de VitD mostram-se promissores na terapia das patologias do tecido ósseo e de suas implicações clínicas.…”

Section: Controleunclassified

Influência da vitamina D na atividade osteoclástica em um modelo de cultura de órgãos ósseos

Ginani¹,

Barboza²

2011

J. Bras. Patol. Med. Lab.

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Introdução: A remodelação óssea é regulada por várias citocinas e hormônios, como a vitamina D3. Essa vitamina, em particular, regula positiva e negativamente a expressão do ligante do receptor ativador do fator nuclear kappa-B (RANKL) e da osteoprotegerina (OPG), respectivamente, e é usada como um indutor da formação de osteoclastos in vitro. Objetivo: Estudar o efeito da vitamina D (VitD) sobre a atividade osteoclástica em cultura de calvárias. Material e método: Fragmentos de calvária de camundongos foram cultivados com meio básico (controle) ou com meio contendo VitD (10 nM: baixa dose; 100 nM: alta dose). Após os intervalos de 24, 48 e 72 horas, o meio de cultura foi coletado para dosagem de cálcio e os fragmentos foram fixados para análise em microscopia confocal. Resultados: Observou-se que a adição de VitD nas duas dosagens promoveu aumento nos níveis de cálcio no meio, porém só foram encontradas diferenças estatisticamente significativas entre alta e baixa dose no intervalo de 24 horas. Na microscopia, foram observadas áreas de desmineralização mais amplas nos fragmentos de calvária cultivados com altas doses de VitD.

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Metabolism of vitamin D3 in human osteoblasts: Evidence for autocrine and paracrine activities of 1α,25-dihydroxyvitamin D3

Cited by 224 publications

References 53 publications

Vitamin D and calcium insufficiency-related chronic diseases: molecular and cellular pathophysiology

Vitamin D and calcium insufficiency-related chronic diseases: molecular and cellular pathophysiology

Ameloblastin is not implicated in bone remodelling and repair

Influência da vitamina D na atividade osteoclástica em um modelo de cultura de órgãos ósseos

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