Premium
1α,25‐Dihydroxyvitamin D 3 decreases DNA binding of nuclear factor‐κB in human fibroblasts
Author(s) -
Harant Hanna,
Wolff Barbara,
Lindley Ivan J.D
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01153-3
Subject(s) - p50 , dna , downregulation and upregulation , microbiology and biotechnology , chromosomal translocation , metabolite , dna binding protein , binding site , chemistry , dna synthesis , transcription factor , calcitriol receptor , biology , gene , biochemistry
1α,25‐Dihydroxyvitamin D 3 (1,25‐(OH) 2 ‐D 3 ), 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 ‐D 3 is dependent on de novo protein synthesis, suggesting that 1,25‐(OH) 2 ‐D 3 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 ‐D 3 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.