1,25-Dihydroxycholecalciferol-Dependent Calcium Uptake by Mouse Mammary Gland in Culture*

Mezzetti, Gabriele; Monti, Maria Giuseppina; Casolo, L. Pernecco; Piccinini, Giulia; Moruzzi, Maria Stella

doi:10.1210/endo-122-2-389

Cited by 56 publications

(17 citation statements)

References 22 publications

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“…In our present study, we found that the preconfluent cells grown in 0.03 mM Ca had an acute Cai response to 2 mM Cao, and this response is further enhanced when cells were treated for 24 h with 1,25(OH) 2 D 3 . A similar effect of 1,25(OH) 2 D 3 on Cai has been observed in other cell systems (Hruska et al, 1988;Bikle, 1990;Pillai et al, 1995;Mozzetti et al, 1988). In these systems, 1,25(OH) 2 D 3 appears to act by increasing agonist-induced phosphatidyl inositol (PI) turnover.…”

Section: Discussionsupporting

confidence: 61%

1,25 dihydroxyvitamin D3 enhances the calcium response of keratinocytes

Ratnam¹,

Bikle²,

Cho³

1999

J. Cell. Physiol.

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The steroid hormone 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) regulates cell proliferation and differentiation. Intracellular calcium (Cai) concentrations play a crucial role in these events. From our previous studies, we have demonstrated a calcium receptor (CaR) in keratinocytes which appears to regulate the initial release of Cai from intracellular stores in response to extracellular calcium (Cao) and so is likely to participate in the differentiation process. In this study, we determined whether the ability of 1,25(OH)2D3 to enhance Ca++ -induced differentiation was mediated at least in part through changes in the CaR. Keratinocytes were grown in keratinocyte growth medium (KGM) with 0.03 mM, 0.1 mM, or 1.2 mM Ca and treated with 10(-8) M 1,25(OH)2D3 till harvest after 5, 7, 14, and 21 days. CaR mRNA levels were quantitated by polymerase chain reaction. The results were compared to the ability of 1,25(OH)2D3 to enhance calcium-stimulated increases in Cai. In cells grown in 0.03 mM Ca, the CaR mRNA levels decreased with time. 1,25(OH)2D3 stimulated the levels at 5 days and prevented the falloff over the subsequent 16 days. On the other hand, in cells grown in 0.1 or 1.2 mM Ca, the message levels remained high, and 1,25(OH)2D3 had no further effect. To study the functional relationship, we harvested cells after 5 and 7 days in culture following a 24 h treatment with 1,25(OH)2D3 or vehicle to measure the Cai response to 2 mM Cao. The preconfluent cells grown in 0.03 mM Ca showed a nearly twofold increase in the Cai response to Cao when pretreated with 1,25(OH)2D3, whereas the confluent cells and those grown in 1.2 mM Ca showed no enhancement by 1,25(OH)2D3. Studies with 45Ca influx into keratinocytes revealed that 1,25(OH)2D3 enhanced the influx in preconfluent and confluent cells when grown in KGM containing 0.03 mM Ca but not in cells grown in 1.2 mM calcium. We conclude that 1,25(OH)2D3 maintains the CaR mRNA levels in cells grown in 0.03 mM Ca, thus maintaining their responsiveness to Cao and so ensuring their ability to differentiate in response to the calcium signal.

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Section: Discussionsupporting

confidence: 61%

1,25 dihydroxyvitamin D3 enhances the calcium response of keratinocytes

Ratnam¹,

Bikle²,

Cho³

1999

J. Cell. Physiol.

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“…Highest levels of VDR in mammary gland are seen during lactation, being maximal at 3 days post partum when the concentration of calcium in milk is highest (Colston et al 1988). Addition of 1,25(OH) 2 D 3 to mammary gland explants increased VDR expression and enhanced calcium uptake (Mezzetti et al 1988). Circulating concentrations of 1,25(OH) 2 D 3 are increased during pregnancy and lactation and recent studies have demonstrated the presence of 1α-hydroxylase in normal breast tissue (Friedrich et al 2000).…”

Section: Vdr Expression In Mammary Tissue and Breast Tumoursmentioning

confidence: 97%

Mechanisms implicated in the growth regulatory effects of vitamin D in breast cancer.

Colston

Hansen²

2002

Endocrine-Related Cancer

223

180

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It is now well established that, in addition to its central role in the maintenance of extracellular calcium levels and bone mineralization, 1,25-dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ), the active form of vitamin D, also acts as a modulator of cell growth and differentiation in a number of cell types, including breast cancer cells. The anti-proliferative effects of 1,25(OH) 2 D 3 have been linked to suppression of growth stimulatory signals and potentiation of growth inhibitory signals, which lead to changes in cell cycle regulators such as p21WAF-1/CIP1 and p27 kip1 , cyclins and retinoblastoma protein as well as induction of apoptosis. Such studies have led to interest in the potential use of 1,25(OH) 2 D 3 in the treatment or prevention of certain cancers. Since this approach is limited by the tendency of 1,25(OH) 2 D 3 to cause hypercalcaemia, synthetic vitamin D analogues have been developed which display separation of the growth regulating effects from calcium mobilizing actions. This review examines mechanisms by which 1,25(OH) 2 D 3 and its active analogues exert both anti-proliferative and pro-apoptotic effects and describes some of the synthetic analogues that have been shown to be of particular interest in relation to breast cancer.

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“…Furthermore, 1,25(OH) 2 D facilitates the cellular uptake of calcium from circulating blood (25). It has been shown that the addition of 1,25(OH) 2 D to mammary gland explants enhances calcium uptake into its functionally differentiated epithelial cells (27). On the other hand, circulating levels of calcium influence the activity of renal 1-a-hydroxylase and thus the circulating concentration of 1,25(OH) 2 D (26).…”

Section: Sources and Metabolismmentioning

confidence: 99%

Vitamin D, Calcium, and Breast Cancer Risk: A Review

Cui

Rohan

2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

156

152

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Vitamin D and calcium are metabolically interrelated and highly correlated dietary factors. Experimental studies have shown their anticarcinogenic effects due to their participation in regulating cell proliferation, differentiation, and apoptosis in normal and malignant breast cells. Given the emerging interest in their potential roles in the etiology of breast cancer, we review the current epidemiologic literature on dietary and/or supplemental intakes of vitamin D, endogenous circulating levels of vitamin D, and dietary and/or supplemental intakes of calcium in relation to breast cancer risk. To place these studies in context, we also provide a brief review of other supporting epidemiologic evidence. Despite inconsistent results from the epidemiologic studies, several lines of evidence suggest that vitamin D and calcium may be involved in the development of breast cancer. Specifically, (a) there is some epidemiologic evidence for inverse associations between vitamin D and calcium intakes and breast cancer; (b) serum, plasma, and/or blood levels of vitamin D metabolites have been inversely associated with breast cancer risk in some studies; (c) high sunlight exposure, presumably reflecting vitamin D synthesis in the skin, has been associated with a reduced risk of breast cancer; (d)

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1,25-Dihydroxycholecalciferol-Dependent Calcium Uptake by Mouse Mammary Gland in Culture*

Cited by 56 publications

References 22 publications

1,25 dihydroxyvitamin D3 enhances the calcium response of keratinocytes

1,25 dihydroxyvitamin D3 enhances the calcium response of keratinocytes

Mechanisms implicated in the growth regulatory effects of vitamin D in breast cancer.

Vitamin D, Calcium, and Breast Cancer Risk: A Review

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