Regulation by dexamethasone and 1,25-dihydroxyvitamin D3 of the 75 kD-type A tumor necrosis factor receptor surface expression and mRNA level in human U937 cells.
1. Dexamethasone selectively reduced the number of the type A (75 kD) receptors whereas 1,25-dihydroxyvitamin D3 reduced the number of both A (75 kD) and B (55 kD) receptors, without any change of their dissociation constants (3-4 x 10(-10) M and 1-2 x 10(-9) M respectively). The level of the type A (75 kD) TNF receptor mRNA was increased following treatment with either steroid. 2. Other agonists which either down-regulated (phorbol dibutyrate) or up-regulated (dibutyryl cAMP and recombinant GM-CSF) rTNF alpha binding also increased the level of this mRNA species. 3. The data suggest that these steroids might alter post-transcriptional event(s).
Chambaut-Guérin
A M
AM
U 282 INSERM, Hormones et Différentiation Cellulaires, Hôpital Henri Mondor, Créteil, France.
Thomopoulos
P
P
D015152:Blotting, Northern; D003994:Bucladesine / Q000494:pharmacology; D002117:Calcitriol / Q000494:pharmacology*; D002460:Cell Line; D004247:DNA / Q000235:genetics; D003907:Dexamethasone / Q000494:pharmacology*; D015870:Gene Expression; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D006801:Humans; D007700:Kinetics; D009693:Nucleic Acid Hybridization; D015240:Phorbol 12,13-Dibutyrate / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism*; D011869:Radioligand Assay; D011956:Receptors, Cell Surface / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor; D011994:Recombinant Proteins / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D018124:Receptors, Tumor Necrosis Factor; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D015240:Phorbol 12,13-Dibutyrate; D003994:Bucladesine; D003907:Dexamethasone; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D004247:DNA; D002117:Calcitriol