Identification of a 1,25-dihydroxyvitamin D3-response element in the 5'-flanking region of the rat calbindin D-9k gene.

Darwish, Hisham M.; DeLuca, Hector F.

doi:10.1073/pnas.89.2.603

Cited by 177 publications

(75 citation statements)

References 43 publications

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“…However, despite the 1,25(OH) 2 D 3 -responsive element in the calbindin-D 9K gene (Darwish & DeLuca 1992), placental calbindin-D 9K expression is not dependent on this hormone (Glazier et al 1995). It seems likely, therefore, that factors other than vitamin D 3 metabolites are involved in activating the renal and placental calbindin genes in diabetic pregnancy.…”

Section: (Oh) 2 Dmentioning

confidence: 89%

Altered calbindin mRNA expression and calcium regulating hormones in rat diabetic pregnancy

Hamilton¹,

Tein²,

Glazier³

et al. 2000

Journal of Endocrinology

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Offspring of rats with diabetes mellitus are at risk of reduced calcium and bone mineral content. Altered expression of the maternal calcium binding proteins, calbindin-D 9K and calbindin-D 28K , which are involved in renal and placental calcium transport, may underlie these problems.We have investigated the effect of diabetes on circulating concentrations of regulatory hormones with respect to calbindin-D mRNA concentrations. Three rat groups were studied; control (CP), streptozotocininduced diabetic (DP), and insulin-treated diabetic (DPI) pregnant rats. Calbindin-D 9K and calbindin-D 28K mRNA abundance in placenta and maternal kidney were measured at days 7, 15, 18 and 21 of gestation, together with serum or plasma concentrations of 1,25 dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ), parathyroid hormone (PTH), PTH-related protein (PTHrP), calcitonin, oestradiol and IGF-I. An increase in placental calbindin-D 9K mRNA abundance between days 18 and 21 in CP and DPI rats was severely blunted in the DP rats. In contrast, renal calbindin-D 28K mRNA abundance was greater at days 7, 15 and 18 in DP compared with CP rats, as was calbindin-D 9K at day 18. Calcitonin concentrations showed no differences between the groups, and both PTH and IGF-I were reduced over the first half of gestation, unlike the calbindins. In contrast, the concentrations of PTHrP and 1,25(OH) 2 D 3 were reduced at term in the DP group compared with the other two groups. Plasma oestradiol concentrations were lower in DP than in CP rats at days 7, 15 and 18, and most striking was the absence in DP rats of the peak of oestradiol seen at day 18 in CP rats. Despite the similarity between changes in placental calbindin mRNA and 1,25(OH) 2 D 3 , previous work has shown placental calbindin-D 9K regulation to be vitamin-D-independent. These studies produce suggestive evidence, therefore, that PTHrP and oestradiol may be involved in the altered calbindin-D expression by kidney and placenta in rat diabetic pregnancy.

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Section: (Oh) 2 Dmentioning

confidence: 89%

Altered calbindin mRNA expression and calcium regulating hormones in rat diabetic pregnancy

Hamilton¹,

Tein²,

Glazier³

et al. 2000

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…31). The identification of two different hormone-responsive elements in the rat calbindin-D,, gene, a 1,25(0H),D3-responsive element (32), and an estrogen-responsive element (33) may confer hormonespecific transcriptional regulation of this gene in different tissues. Indeed, the expression of the calbindin-D,, gene in rat intestine is regulated by 1,25(OH),D3 and not by estrogen (34,35) whereas in rat uterus it appears to be regulated by estrogen (33,35,36) and not by 1,25(OH),D3 (34).…”

Section: Discussionmentioning

confidence: 99%

Calbindin-D9K Gene Expression in Rat Chorioallantoic Placenta Is Not Regulated by 1,25-Dihydroxyvitamin D3

1995

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“…Furthermore, recent results suggest that AP-1 also binds to the sequence TGAACGG in the middle of the VDR-binding motifs . Composite AP-1 +VDRE element is not a general characteristic of VDR-regulated bone proteins, e.g., VDRE of the rat calbindin D-9k gene does not contain a binding site for AP-1 (Darwish and DeLuca, 1992).…”

mentioning

confidence: 99%

Functional Interference Between AP‐1 and the Vitamin D Receptor on Osteocalcin Gene Expression in Human Osteosarcoma Cells

Jääskeläinen

Pirskanen

Ryhänen

et al. 1994

European Journal of Biochemistry

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The binding of transcription factor AP-1 and vitamin D receptor (VDR) to the composite AP-1 plus vitamin-D-responsive promoter region (AP-1 +VDRE) of the human osteocalcin gene was characterized in osteocalcin-producing (MG-63) and non-producing (U2-0s, SaOs-2) human osteosarcoma cell lines. In mobility-shift assays with AP-1 +VDRE, AP-1, and VDRE probes and nuclear extracts from these cells, one AP-1-specific and two VDR-specific (fast and slow mobility) interactions were observed. Characterization of the complexes indicated that AP-1 and VDR do not bind simultaneously to the AP-1 + VDRE oligonucleotide. Intensity of the complexes was greatly influenced by cell density: in MG-63 and SaOs-2 cells, AP-1 binding was strong during the proliferative period disappearing at confluency whereas, in U2-0s cells, AP-1 binding was prominent also at the confluent stage. Furthermore, MG-63 cells possessed the faster migrating VDR complex at all stages of confluency whereas, in U2-0s and SaOs-2 cells, it was very weak or absent. There were no detectable differences in the levels of VDR protein between these cell lines. In U2-0s cells, the level of c-jun mRNA was higher than in the other two cell lines, whereas none of these cell lines exhibited detectable levels of c-fos mRNA at the confluent stage. Exogenous c-Jun protein effectively blocked the VDR-DNA interaction. Further, all these cell lines expressed mRNA for retinoid X receptor a (RXRa), the factor suggested to be required for the VDR-DNA interaction. The presence of an accessory factor in the VDR-DNA complexes was indirectly shown by treatment of the cells with 9-cis retinoic acid and by cycloheximide. Both treatments reduced VDR binding without affecting the VDR protein level. These results suggest that AP-1 interferes with VDR binding to the AP-1+VDRE element and that the vitamin D responsiveness of the osteocalcin gene correlates with weak AP-1 binding and strong binding of the faster migrating VDR complex.

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Identification of a 1,25-dihydroxyvitamin D3-response element in the 5'-flanking region of the rat calbindin D-9k gene.

Cited by 177 publications

References 43 publications

Altered calbindin mRNA expression and calcium regulating hormones in rat diabetic pregnancy

Altered calbindin mRNA expression and calcium regulating hormones in rat diabetic pregnancy

Calbindin-D9K Gene Expression in Rat Chorioallantoic Placenta Is Not Regulated by 1,25-Dihydroxyvitamin D3

Functional Interference Between AP‐1 and the Vitamin D Receptor on Osteocalcin Gene Expression in Human Osteosarcoma Cells

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