Soluble glucocorticoid-induced tumor necrosis factor receptor stimulates osteoclastogenesis by down-regulation of osteoprotegerin in bone marrow stromal cells

Bone ◽  
2006 ◽  
Vol 39 (4) ◽  
pp. 716-723 ◽  
Author(s):  
Hyun-Hee Shin ◽  
Soo-Jin Kim ◽  
So-Young Kang ◽  
Dong-Sul Lee ◽  
Hye-Seon Choi
Keyword(s):  
Bone Marrow ◽  
Tumor Necrosis Factor ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Marrow Stromal Cells ◽  
Down Regulation ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor induces rapid down-regulation of TXNIP in human T cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Trine B. Levring ◽  
Martin Kongsbak-Wismann ◽  
Anna K. O. Rode ◽  
Fatima A. H. Al-Jaberi ◽  
Daniel V. Lopez ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
Glucose Uptake ◽  
Tumor Necrosis ◽  
Gradient Centrifugation ◽  
Tumor Necrosis Factor Receptor ◽  
Down Regulation ◽  
Interacting Protein ◽  
Human T Cells ◽  
Necrosis Factor

Abstract In addition to antigen-driven signals, T cells need co-stimulatory signals for robust activation. Several receptors, including members of the tumor necrosis factor receptor superfamily (TNFRSF), can deliver co-stimulatory signals to T cells. Thioredoxin interacting protein (TXNIP) is an important inhibitor of glucose uptake and cell proliferation, but it is unknown how TXNIP is regulated in T cells. The aim of this study was to determine expression levels and regulation of TXNIP in human T cells. We found that naïve T cells express high levels of TXNIP and that treatment of blood samples with TNF results in rapid down-regulation of TXNIP in the T cells. TNF-induced TXNIP down-regulation correlated with increased glucose uptake. Furthermore, we found that density gradient centrifugation (DGC) induced down-regulation of TXNIP. We demonstrate that DGC induced TNF production that paralleled the TXNIP down-regulation. Treatment of blood with toll-like receptor (TLR) ligands induced TNF production and TXNIP down-regulation, suggesting that damage-associated molecular patterns (DAMPs), such as endogenous TLR ligands, released during DGC play a role in DGC-induced TXNIP down-regulation. Finally, we demonstrate that TNF-induced TXNIP down-regulation is dependent on caspase activity and is caused by caspase-mediated cleavage of TXNIP.

Bone marrow stromal cells promote growth and survival of prostate cancer cells

2007 ◽  
Vol 35 (4) ◽  
pp. 698-700 ◽  
Author(s):  
N.A. Cross ◽  
M. Papageorgiou ◽  
C.L. Eaton
Keyword(s):  
Prostate Cancer ◽  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Marrow Stromal Cells ◽  
Cancer Cell Proliferation ◽  
Growth And Survival ◽  
Prostate Cancers ◽  
Necrosis Factor ◽  
Insulin Like Growth Factors

Prostate cancers frequently metastasize to the skeleton, and it has been hypothesized that this environment selectively supports the growth of these tumours. Specifically there is strong evidence that interactions between tumour cells and BMSCs (bone marrow stromal cells) play a major role in supporting prostate cancer growth and survival in bone. Here, we examine factors shown to be secreted by BMSCs, such as IGFs (insulin-like growth factors) and IL-6 (interleukin 6), shown to promote prostate cancer cell proliferation and to potentially replace the requirement for androgens. In addition we discuss another factor produced by BMSCs, osteoprotegerin, which may promote tumour cell survival by suppressing the biological activity of the pro-apoptotic ligand TRAIL (tumour-necrosis-factor-related apoptosis-inducing ligand).

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.

TUMOR NECROSIS FACTOR RECEPTOR REGULATION OF BONE MARROW CELL APOPTOSIS DURING ENDOTOXIN-INDUCED SYSTEMIC INFLAMMATION

Shock ◽  
2006 ◽  
Vol 25 (5) ◽  
pp. 464-471 ◽  
Author(s):  
Joji Kotani ◽  
Nicholas J. Avallone ◽  
Edward Lin ◽  
Masahiro Goshima ◽  
Stephen F. Lowry ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Tumor Necrosis Factor ◽  
Bone Marrow Cell ◽  
Systemic Inflammation ◽  
Cell Apoptosis ◽  
Tumor Necrosis ◽  
Marrow Cell ◽  
Tumor Necrosis Factor Receptor ◽  
Receptor Regulation ◽  
Necrosis Factor
Sign in / Sign up

Export Citation Format

Share Document