1α,25‐Dihydroxyvitamin D3 decreases DNA binding of nuclear factor‐κB in human fibroblasts

FEBS Letters

Harant, Hanna²  Lindley, Ivan J.D²  Wolff, Barbara¹ 

[1] Department of Chemistry and Pharmacology, Novartis Research Institute, A-1235 Vienna, Austria;Department of Cellular and Molecular Biology, Novartis Research Institute, Brunner Strasse 59, A-1235 Vienna, Austria

关键词: 1α;    25-Dihydroxyvitamin D3;    Fibroblast;    Interleukin-8;    Nuclear factor-κB;    Tumor necrosis factor-α;    1;    25-(OH)2-D3;    1α;    25-dihydroxyvitamin D3;    CHX;    cycloheximide;    EMSA;    electrophoretic mobility shift assay;    IL-1β;    interleukin-1β;    IL-6;    interleukin-6;    IL-8;    interleukin-8;    NF-κB;    nuclear factor-κB;    TNF-α;    tumor necrosis factor-α;   

DOI  :  10.1016/S0014-5793(98)01153-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

1α,25-Dihydroxyvitamin D₃ (1,25-(OH)₂-D₃), the active metabolite of vitamin D, can inhibit NF-κB activity in human MRC-5 fibroblasts, targeting DNA binding of NF-κB but not translocation of its subunits p50 and p65. The partial inhibition of NF-κB DNA binding by 1,25-(OH)₂-D₃ is dependent on de novo protein synthesis, suggesting that 1,25-(OH)₂-D₃ may regulate expression of cellular factors which contribute to reduced DNA binding of NF-κB. Although NF-κB binding is decreased by 1,25-(OH)₂-D₃ in MRC-5 cells, IL-8 and IL-6 mRNA levels are only moderately downregulated, demonstrating that inhibition of NF-κB DNA binding alone is not sufficient for optimal downregulation of these genes.

【 授权许可】

Unknown