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  • 1
    Electronic Resource
    Electronic Resource
    All-trans retinoic acid inhibits binding of 1,25-dihydroxy-vitamin D3 to the vitamin D receptor in cultured human keratinocytes (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Experimental dermatology 5 (1996), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract Psoriasis is characterized by hyperproliferation and impared differentiation of epidermal keratinocytes (KCs). Psoriasis can be treated with derivatives of relinoic acid (RA) and vitamin D3. Analogues of vitamin D3 are able to inhibit proliferation and stimulate differentiation of KCs. In contrast, RA inhibits terminal differentiation of KCs. Interactions are known to occur between RA and vitamin D3 signalling pathways. The purpose of the present study was to determine the effect of all-trans RA on the binding of 1,25-dihydroxy-vitamin D3 (1,25 (OH)2D3) to the vitamin D3, receptor (VDR) of cultured human KCs. Cultured KCs from normal adults were incubated with or without RA (10−9–10−7 M) for 4-24 h. Cells were then harvested, homogenized and ultrasonicated. The extracted protein was incubated with 3H-1,25 (OH)2D3 (0.015-1.0 nM) with or without 250-fold excess nonradioactive 1,25 (OH)2D3 for 24 h and specific binding was determined by use of the dextran coated charcoal binding assay. Western blot analysis utilizing the monoclonal antibody 9A7γ to VDR was performed on protein extracted from the KCs. The bands resulting from Western blot analysis were visualized by enhanced chemiluminescence. From Scatchard analysis it was found that KCs bind 1,25 (OH)2D3 with high affinity (Kd = 0.175 nM). This binding was dose and time dependently inhibited by RA (60% inhibition at 10−7 M after 24 h of incubation). By Western blot analysis, RA had no effect on the amount of protein extracted from KCs at any of the RA concentrations tested. In conclusion, these results show that binding of vitamin D3 to its receptor of human KCs can be inhibited markedly by RA without effecting the amount of protein. These results are in contrast to results with other cell types in which RA upregulates binding of 1,25 (OH)2D3 to the VDR. Because interaction between retinoids and vitamin D3 may occur at different levels during signal trans-duction, it is not possible to predict from our results whether RA will inhibit the effects of vitamin D3, in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0625.1996.tb00089.x
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  • 2
    Electronic Resource
    Electronic Resource
    Upregulation of vitamin D receptor levels by 1,25(OH)2 vitamin D3 in cultured human keratinocytes (1997)
    Springer
    Archives of dermatological research 289 (1997), S. 367-372 
    Details
    ISSN: 1432-069X
    Keywords: Key words 1 ; 25-Dihydroxyvitamin D3 ; Vitamin D ; receptor ; Keratinocytes ; Vitamin D receptor mRNA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The natural biologically active form of vitamin D3, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), possesses antiproliferative, prodifferentiating and immunomodulatory properties. The actions of 1,25(OH)2D3 are mediated through the intracellular vitamin D receptor (VDR), and the level of VDR is believed to determine the cellular responsiveness to vitamin D3. In the present study we examined the effects of 1,25(OH)2D3 on the expression of VDR and its message in cultured human keratinocytes. Western analysis showed the mean VDR content to be higher in undifferentiated cultures (175 pg/μg protein) than in differentiated cultures (90 pg/μg protein). Incubation with 1,25(OH)2D3 induced an increase in the VDR in both undifferentiated and differentiated keratinocytes. The VDR increase was detectable after 2 h and maximal (approximately two-fold stimulation) after 8 h. The 1,25(OH)2D3-induced stimulation of VDR levels was dose dependent with a maximum at 10–7 M. The VDR mRNA levels as determined by the ribonuclease protection assay showed a peak (50% stimulation) after approximately 2 h. Although this increase in VDR mRNA was not statistically significant, the results indicate that the ligand-induced upregulation of VDR involves increased transcription. The upregulation of VDR levels may increase the responsiveness to 1,25(OH)2D3 and may, therefore, be an important mechanism for regulating the effects of 1,25(OH)2D3 on keratinocyte proliferation and differentiation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004030050206
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    Paper (German National Licenses)
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