Inhibition of the 1,25-Dihydroxyvitamin D3-Induced Increase in Vitamin D Receptor (VDR) Levels and Binding of VDR-Retinoid X Receptor (RXR) to a Direct Repeat (DR)-3 Type Response Element by an RXR-Specific Ligand in Human Keratinocyte Cultures

Jensen, Tina Jellesmark; Henriksen, Linda Ø; Sølvsten, Henrik; Kragballe, Knud

doi:10.1016/s0006-2952(97)00580-7

Cited by 10 publications

(11 citation statements)

References 26 publications

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“…Confirming a previous report [18], 1,25D 3 rapidly induced VDR expression in keratinocytes (Fig. 4A), and stimulated the protein binding to the DR-3 element (Fig.…”

Section: Transfection With Dn-pparg Does Not Affect Binding Of the Drsupporting

confidence: 93%

PPARγ mediates innate immunity by regulating the 1α,25-dihydroxyvitamin D3 induced hBD-3 and cathelicidin in human keratinocytes

Dai

Sayama

Tohyama

et al. 2010

Journal of Dermatological Science

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“…Confirming a previous report [18], 1,25D 3 rapidly induced VDR expression in keratinocytes (Fig. 4A), and stimulated the protein binding to the DR-3 element (Fig.…”

Section: Transfection With Dn-pparg Does Not Affect Binding Of the Drsupporting

confidence: 93%

PPARγ mediates innate immunity by regulating the 1α,25-dihydroxyvitamin D3 induced hBD-3 and cathelicidin in human keratinocytes

Dai

Sayama

Tohyama

et al. 2010

Journal of Dermatological Science

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“…[24][25][26][27][28][29][30][31][32] However, multiple forms of vitamin A have also been shown to exert antagonistic effects on certain vitamin D actions, including serum calcium elevation and bone resorption. [33][34][35][36] The combinatorial effects of 1,25D and 9cRA against lung carcinogenesis in vivo have not been investigated.…”

mentioning

confidence: 99%

Inhibition of lung carcinogenesis by 1α,25‐dihydroxyvitamin D₃ and 9‐cis retinoic acid in the A/J mouse model: Evidence of retinoid mitigation of vitamin D toxicity

Mernitz

Smith

Wood

et al. 2007

Intl Journal of Cancer

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9-cis-Retinoic acid (9cRA) and 1a, 25-dihydroxyvitamin D 3 (1,25D) show promise as potential chemopreventive agents. We examined 9cRA and 1,25D, alone and in combination, for their potential to inhibit carcinogen (NNK)-induced lung carcinogenesis in A/J mice. A/J mice (n 5 14/group) were treated with 9cRA (7.5, 15, or 30 mg/kg diet), 1,25D (2.5 or 5.0 lg/kg diet), or a combination of 9cRA (15 mg/kg diet) plus 1,25D (2.5 lg/kg diet) for 3 weeks before and 17 weeks after carcinogen injection. Lung tumor incidence, tumor multiplicity, plasma 1,25D levels and kidney expression of vitamin D 24-hydroxylase (CYP24) were determined. Compared to carcinogen-injected controls, mice receiving 9cRA supplementation had significantly lower tumor multiplicity at all doses (decreased 68-85%), with body weight loss at the higher doses of 9cRA. Mice receiving 1,25D supplementation had significantly lower tumor incidence (decreased 36 and 82%) and tumor multiplicity (decreased 85 and 98%), but experienced significant body weight loss, kidney calcium deposition, elevated kidney CYP24 expression and decreased fasting plasma 1,25D levels. Although, there was no apparent influence on chemopreventive efficacy, addition of 9cRA to 1,25D treatment effectively prevented the weight loss and kidney calcification associated with 1,25D treatment alone. These data demonstrate that 9cRA and 1,25D, alone or combined, can inhibit lung tumor promotion in the A/J mouse model. Combining 1,25D with 9cRA has the potential to mitigate the toxicity of 1,25D, while preserving the significant effect of 1,25D treatment against lung carcinogenesis. The underlying mechanism behind this effect does not appear to be related to retinoid modulation of vitamin D catabolism. ' 2006 Wiley-Liss, Inc.Key words: lung cancer; 9-cis retinoic acid; 1a,25-dihydroxyvitamin D 3Chemoprevention by diet or drug intervention may offer a realistic and practical means of modifying the risk of lung cancer, the leading cause of cancer deaths in both men and women in the United States. 1 Two classes of chemopreventive compounds that have been considered are the retinoids and the active form of vitamin D, 1a,25-dihydroxyvitamin D 3 (1,25D, also calcitriol).Retinoids are required for proper differentiation of lung and upper airway epithelium, 2 and both 9-cis retinoic acid (9cRA, also 9-cis tretinoin) and all-trans retinoic acid have been shown to inhibit cell growth and proliferation in lung cancer cell lines. 3 Studies in animal models of lung cancer suggest that retinoids may be effective in cancer chemoprevention in vivo, but results have varied with species, dose and timing of treatment in relation to induction of carcinogenesis. [4][5][6] In human lung cancer, epidemiological evidence supports a role for vitamin A-rich foods and supplements in protection against the development of lung cancer in smokers and nonsmokers alike 7 ; however, clinical trials assessing the efficacy of retinoid supplementation against lung cancer have yielded inconsistent and inconclusive results. [8][...

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“…It has been suggested that the therapeutic effect of topically applied vitamin D 3 in psoriasis correlates with the induced increase of the VDR mRNA levels 15 . Furthermore, the levels of VDR have been described to correlate with the VDR binding to VDRE both in cultured human keratinocytes 14 and in normal human skin (unpublished data). These results are supported by the present study showing a strong linear correlation between VDR (involved/uninvolved) and VDRE (involved/uninvolved).…”

Section: Discussionmentioning

confidence: 90%

“…was added, and incubation was continued for 30 min at room temperature. Protein‐bound DNA was separated by the free probe and quantified as previously described 14 …”

Section: Methodsmentioning

confidence: 99%

The vitamin D₃receptor and retinoid X receptors in psoriatic skin: the receptor levels correlate with the receptor binding to DNA

Jensen

Sørensen

Sølvsten

et al. 1998

British Journal of Dermatology

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It is unknown whether vitamin D3 analogues improve psoriasis by overcoming an intrinsic abnormality of the vitamin D3 signalling pathway in psoriatic skin. The effects of vitamin D3 are mediated through the vitamin D3 receptor (VDR). The VDR heterodimerizes with another transcriptional regulator, preferentially the retinoid X receptor (RXR). In the present study the levels of VDR and RXR in involved and uninvolved psoriatic skin were determined by immunoblotting, and the binding of the VDR-RXR complex to a vitamin D3 response element (VDRE) consisting of two hexanucleotides spaced by three nucleotides (DR-3) by the electrophoretic mobility shift assay. The levels of VDR were similar in involved and uninvolved skin. RXR alpha, but neither RXR beta nor RXR gamma, was detectable. The RXR alpha levels were slightly lower in involved psoriatic skin than in uninvolved psoriatic skin, but this difference was statistically insignificant. The binding of VDR-RXR to the DR-3 VDRE was similar in uninvolved and involved psoriatic skin. Furthermore, there was a strong linear correlation between the levels of both VDR and RXR alpha and their binding to DNA. In conclusion, the initial part of the vitamin D3 signalling pathway involving receptor levels and receptor binding to DNA is normal in involved psoriatic skin.

show abstract

Inhibition of the 1,25-Dihydroxyvitamin D3-Induced Increase in Vitamin D Receptor (VDR) Levels and Binding of VDR-Retinoid X Receptor (RXR) to a Direct Repeat (DR)-3 Type Response Element by an RXR-Specific Ligand in Human Keratinocyte Cultures

Cited by 10 publications

References 26 publications

PPARγ mediates innate immunity by regulating the 1α,25-dihydroxyvitamin D3 induced hBD-3 and cathelicidin in human keratinocytes

PPARγ mediates innate immunity by regulating the 1α,25-dihydroxyvitamin D3 induced hBD-3 and cathelicidin in human keratinocytes

Inhibition of lung carcinogenesis by 1α,25‐dihydroxyvitamin D₃ and 9‐cis retinoic acid in the A/J mouse model: Evidence of retinoid mitigation of vitamin D toxicity

The vitamin D₃receptor and retinoid X receptors in psoriatic skin: the receptor levels correlate with the receptor binding to DNA

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Inhibition of the 1,25-Dihydroxyvitamin D3-Induced Increase in Vitamin D Receptor (VDR) Levels and Binding of VDR-Retinoid X Receptor (RXR) to a Direct Repeat (DR)-3 Type Response Element by an RXR-Specific Ligand in Human Keratinocyte Cultures

Cited by 10 publications

References 26 publications

PPARγ mediates innate immunity by regulating the 1α,25-dihydroxyvitamin D3 induced hBD-3 and cathelicidin in human keratinocytes

PPARγ mediates innate immunity by regulating the 1α,25-dihydroxyvitamin D3 induced hBD-3 and cathelicidin in human keratinocytes

Inhibition of lung carcinogenesis by 1α,25‐dihydroxyvitamin D3 and 9‐cis retinoic acid in the A/J mouse model: Evidence of retinoid mitigation of vitamin D toxicity

The vitamin D3receptor and retinoid X receptors in psoriatic skin: the receptor levels correlate with the receptor binding to DNA

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Inhibition of lung carcinogenesis by 1α,25‐dihydroxyvitamin D₃ and 9‐cis retinoic acid in the A/J mouse model: Evidence of retinoid mitigation of vitamin D toxicity

The vitamin D₃receptor and retinoid X receptors in psoriatic skin: the receptor levels correlate with the receptor binding to DNA