Mouse Gene Set: NEMETH_INFLAMMATORY_RESPONSE_LPS_UP

For the Human gene set with the same name, see NEMETH_INFLAMMATORY_RESPONSE_LPS_UP

Standard name NEMETH_INFLAMMATORY_RESPONSE_LPS_UP
Systematic name MM1152
Brief description Genes up-regulated in RAW 264.7 cells (macrophage) 3 hr after stimulation with bacterial lipopolysaccharide (LPS).
Full description or abstract Adenosine is released into the extracellular space from nerve terminals and cells subjected to ischemic stress. This nucleoside modulates a plethora of cellular functions via occupancy of specific receptors. Adenosine is also an important endogenous regulator of macrophage function, because it suppresses the production of a number of proinflammatory cytokines by these cells. However, the mechanisms of this anti-inflammatory effect have not been well characterized. We hypothesized that adenosine may exert some of its anti-inflammatory effects by decreasing activation of the transcription factor nuclear factor-kappaB (NF-kappaB), because gene expression of most of the proinflammatory cytokines inhibited by adenosine is dependent on NF-kappaB activation. Using bacterial lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages, we found that adenosine as well as adenosine receptor agonists decreased the production of tumor necrosis factor (TNF)-alpha, a typical NF-kappaB-regulated cytokine. This effect of adenosine was not due to an action on the process of TNF-alpha release, because adenosine suppressed also the intracellular levels of TNF-alpha. However, cDNA microarray analysis revealed that mRNA levels of neither TNF-alpha nor other cytokines were altered by adenosine in either LPS-activated or quiescent macrophages. In addition, although LPS induced expression of a number of other, noncytokine genes, including the adenosine A2b receptor, adenosine did not affect the expression of these genes. Furthermore, adenosine as well as adenosine receptor agonists failed to decrease LPS-induced NF-kappaB DNA binding, NF-kappaB promoter activity, p65 nuclear translocation, and inhibitory kappaB degradation. Together, our results suggest that the anti-inflammatory effects of adenosine are independent of NF-kappaB.
Collection M2: Curated
      CGP: Chemical and Genetic Perturbations
Source publication Pubmed 12766259   Authors: Németh ZH,Leibovich SJ,Deitch EA,Vizi ES,Szabó C,Hasko G
Exact source Table 1: LPS/Control
Related gene sets (show 1 additional gene sets from the source publication)
External links
Filtered by similarity ?
Source species Mus musculus
Contributed by Kevin Vogelsang (MSigDB Team)
Source platform or
identifier namespace
MOUSE_SEQ_ACCESSION
Dataset references  
Download gene set format: grp | gmt | xml | json | TSV metadata
Compute overlaps ? (show collections to investigate for overlap with this gene set)
Compendia expression profiles ? NG-CHM interactive heatmaps
(Please note that clustering takes a few seconds)
Mouse Transcriptomic BodyMap compendium

Legacy heatmaps (PNG)
Mouse Transcriptomic BodyMap compendium
Advanced query Further investigate these 90 genes
Show members (show 98 source identifiers mapped to 90 genes)
Version history 2022.1.Mm: First Introduced.

See MSigDB license terms here. Please note that certain gene sets have special access terms.