scholarly journals Regulation of macrophage function in tumors: the multifaceted role of NF-κB

Blood ◽  
2009 ◽  
Vol 113 (14) ◽  
pp. 3139-3146 ◽  
Author(s):  
Thorsten Hagemann ◽  
Subhra K. Biswas ◽  
Toby Lawrence ◽  
Antonio Sica ◽  
Claire E. Lewis
Keyword(s):  
Transcription Factor ◽  
Tumor Cells ◽  
Tumor Development ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Invasion And Metastasis ◽  
Exact Role ◽  
Cellular Processes ◽  
Transcription Factor Nuclear Factor

Abstract The pivotal role of tumor-associated macrophages (TAMs) in tumor progression is now well established. TAMs have been shown to influence multiple steps in tumor development including the growth, survival, invasion, and metastasis of tumor cells as well as angiogenesis and lymphangiogenesis in tumors. The molecular circuits that polarize TAMs toward such a protumoral phenotype are now the focus of intense investigation. The transcription factor, nuclear factor–κB (NF-κB), is a master regulator of many cellular processes and been shown to regulate various pathways that impact on the function of TAMs. Much evidence for this has come from the use of elegant transgenic murine tumor models in which modification of single components of the NF-κB signaling pathway has been shown to regulate the pro-tumor repertoire of TAMs. Here, we outline this evidence and attempt to reconcile the various views that have emerged recently over the exact role of NF-κB in this phenomenon.

Spontaneous, homeostatic, and inflammation-induced sleep in NF-κB p50 knockout mice

2006 ◽  
Vol 291 (5) ◽  
pp. R1516-R1526 ◽  
Author(s):  
K. A. Jhaveri ◽  
V. Ramkumar ◽  
R. A. Trammell ◽  
L. A. Toth
Keyword(s):  
Transcription Factor ◽  
Influenza Virus ◽  
Slow Wave Sleep ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Immune Challenge ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Transcription Factor Nuclear Factor

The dimeric transcription factor nuclear factor-κB (NF-κB) regulates several endogenous sleep-modulatory substances and thereby serves as a pivotal mediator of sleep-wake homeostasis. To further define the role of NF-κB in sleep regulation, we monitored sleep and temperature in mice that lack the p50 subunit of NF-κB [p50 knockout (KO) mice]. Compared with the control B6129PF2/J strain, p50 KO mice spend more time in slow-wave sleep (SWS) and rapid eye movement sleep (REMS) under normal conditions and show enhanced homeostatic recovery of sleep after sleep loss. p50 KO mice also show increased SWS and reduced REMS and temperature after the administration of lipopolysaccharide, yet they are behaviorally less responsive to challenge with influenza virus. These data support a role for NF-κB, and, in particular, for the p50 subunit, in the regulation of sleep in healthy mice and in mice experiencing immune challenge.

The use of siRNA as a pharmacological tool to assess a role for the transcription factor NF-IL6 in the brain under in vitro and in vivo conditions during LPS-induced inflammatory stimulation

2017 ◽  
Vol 28 (6) ◽  
Author(s):  
Jelena Damm ◽  
Joachim Roth ◽  
Rüdiger Gerstberger ◽  
Christoph Rummel
Keyword(s):  
Transcription Factor ◽  
Brain Cells ◽  
Nuclear Factor ◽  
Si Rna ◽  
The Brain ◽  
Deficient Mice ◽  
Transcription Factor Nuclear Factor

AbstractBackground:Studies with NF-IL6-deficient mice indicate that this transcription factor plays a dual role during systemic inflammation with pro- and anti-inflammatory capacities. Here, we aimed to characterize the role of NF-IL6 specifically within the brain.Methods:In this study, we tested the capacity of short interfering (si) RNA to silence the inflammatory transcription factor nuclear factor-interleukin 6 (NF-IL6) in brain cells underResults:In cells of a mixed neuronal and glial primary culture from the ratConclusions:This approach was, thus, not suitable to characterize the role NF-IL6 in the brain

scholarly journals NFAT5 Contributes to Osmolality-Induced MCP-1 Expression in Mesothelial Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Christoph Küper ◽  
Franz-X. Beck ◽  
Wolfgang Neuhofer
Keyword(s):  
Transcription Factor ◽  
Mesothelial Cell ◽  
Nuclear Factor Κb ◽  
Mesothelial Cells ◽  
Nuclear Factor ◽  
Peritoneal Fibrosis ◽  
Activated T Cells ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Transcription Factor Nuclear Factor

Increased expression of the C-C chemokine monocyte chemoattractant protein-1 (MCP-1) in mesothelial cells in response to high glucose concentrations and/or high osmolality plays a crucial role in the development of peritoneal fibrosis during continuous ambulatory peritoneal dialysis (CAPD). Recent studies suggest that in kidney cells osmolality-induced MCP-1 upregulation is mediated by the osmosensitive transcription factor, nuclear factor of activated T cells 5 (NFAT5). The present study addressed the question of whether activation of NFAT5 by hyperosmolality, as present in PD fluids, contributes to MCP-1 expression in the mesothelial cell line Met5A. Hyperosmolality, induced by addition of glucose, NaCl, or mannitol to the growth medium, increased NFAT5 activity and stimulated MCP-1 expression in Met5A cells. siRNA-mediated knockdown of NFAT5 attenuated osmolality-induced MCP-1 upregulation substantially. Hyperosmolality also induced activation of nuclear factor-κB (NF-κB). Accordingly, pharmacological inhibition of NF-κB significantly decreased osmolality-induced MCP-1 expression. Taken together, these results indicate that high osmolalities activate the transcription factor NFAT5 in mesothelial cells. NFAT5 in turn upregulates MCP-1, likely in combination with NF-κB, and thus may participate in the development of peritoneal fibrosis during CAPD.

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