Production of interleukin-6 in human osteoblasts and human bone marrow stromal cells: evidence that induction by interleukin-1 and tumor necrosis factor-alpha is not regulated by ovarian steroids.

Endocrinology ◽  
1995 ◽  
Vol 136 (9) ◽  
pp. 4056-4067 ◽  
Author(s):  
L Rifas ◽  
J S Kenney ◽  
M Marcelli ◽  
R Pacifici ◽  
S L Cheng ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Marrow Stromal Cells ◽  
Necrosis Factor Alpha ◽  
Human Osteoblasts ◽  
Ovarian Steroids ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Recombinant tumor necrosis factor alpha and interleukin 1 alpha increase expression of c-abl protooncogene mRNA in cultured human marrow stromal cells

1989 ◽  
Vol 86 (17) ◽  
pp. 6788-6792 ◽  
Author(s):  
D F Andrews ◽  
J J Nemunaitis ◽  
J W Singer
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Stromal Cells ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Marrow Stromal Cells ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Recombinant Tumor Necrosis Factor ◽  
Necrosis Factor

Analysis of protooncogene RNA expression in marrow stromal cells from long-term marrow culture demonstrated high levels of c-abl 5-, 6-, and 7-kilobase (kb) RNA transcripts. In experiments on three independently derived simian virus 40-transformed marrow stromal cell lines, the expression of these c-abl transcripts was further increased in response to recombinant tumor necrosis factor alpha (1000 units/ml) and interleukin 1 alpha (10 units/ml). Although lymphocyte-conditioned medium predominantly up-regulated the 5-kb transcript, interleukin 1 alpha primarily affected the 6-kb transcript. The up-regulation of the 5-kb c-abl message correlated with up-regulation of the granulocyte/macrophage colony-stimulating factor transcript and down-regulation of procollagen I transcripts in transformed cells. These data suggest that c-abl plays roles in the regulation of extracellular matrix expression and in the regulation of hematopoietic growth factors by stromal cells.

Pancreatic beta-cell-selective production of tumor necrosis factor-alpha induced by interleukin-1

Diabetes ◽  
1993 ◽  
Vol 42 (7) ◽  
pp. 1026-1031 ◽  
Author(s):  
K. Yamada ◽  
N. Takane ◽  
S. Otabe ◽  
C. Inada ◽  
M. Inoue ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Beta Cell ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Pancreatic Beta Cell ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

NF-IL6 and AP-1 cooperatively modulate the activation of the TSG-6 gene by tumor necrosis factor alpha and interleukin-1

1994 ◽  
Vol 14 (10) ◽  
pp. 6561-6569
Author(s):  
L Klampfer ◽  
T H Lee ◽  
W Hsu ◽  
J Vilcek ◽  
S Chen-Kiang
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Human Fibroblasts ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Normal Human ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1) activate transcription of the TSG-6 gene in normal human fibroblasts through a promoter region (-165 to -58) that encompasses an AP-1 and a NF-IL6 site. We show by deletion analysis and substitution mutagenesis that both sites are necessary for activation by TNF-alpha. Activation by IL-1 requires the NF-IL6 site and is enhanced by the AP-1 site. These results suggest that the NF-IL6 and AP-1 family transcription factors functionally cooperate to mediate TNF-alpha and IL-1 signals. Consistent with this possibility, IL-1 and TNF-alpha markedly increase the binding of Fos and Jun to the AP-1 site, and NF-IL6 activates the native TSG-6 promoter. Activation by NF-IL6 requires an intact NF-IL6 site and is modulated by the ratio of activator to inhibitor NF-IL6 isoforms that are translated from different in-frame AUGs. However, the inhibitor isoform can also bind to the AP-1 site and repress AP-1 site-mediated transcription. The finding that the inhibitor isoform antagonizes activation of the native TSG-6 promoter by IL-1 and TNF-alpha suggests that NF-IL6 has a physiologic role in these cytokine responses. Thus, the functionally distinct NF-IL6 isoforms cooperate with Fos and Jun to positively and negatively regulate the native TSG-6 promoter by TNF-alpha and IL-1.

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