Transcriptomic changes in RAW264.7 cells exposed to bacterial lipopolysaccharide (LPS) and/or the nitrone compound 5,5-dimethyl-1-pyrroline N-oxide (DMPO) - Ilumina Microarray data

The main hypothesis to be tested is that DMPO causes transcriptomic changes in macrophages (RAW264.7 cell line) to make them resistant to activation with bacterial lipopolysaccharide (LPS) , chromatographically purified from E. coli 055:B5.
The main objective was to characterize the overall trasncriptomic changes caused in RAW264.7 cells exposed to DMPO and/or LPS.
RAW264.7 cells (ATCC TIB-71, passage 3-4) were cultured in T-25 flask in DMEM culture medium with high glucose and 5% heat inactivated fetal calf serum (GIBCO). After reaching a 70% confluence, monolayers were rinsed and incubated in medium alone, medium+DMPO (50mM), medium+LPS (1ng/ml), medium+DMPO+LPS. After incubation for 6h, in 5% CO2 at 37oC, under the 4 different conditions the medium was removed, the mnolayers rinsed with PBS. Following the cell monolayers were harvested in 1ml TRIZOL to purify total RNA. RNA integrity was assessed by capilar electrophoresis (Eukaryote Total RNA Nano). This experiment was repeated in 3 different dates (3 replicates). Transcriptomic analisis was performed by microarray in a Ilumina Platform.
This data set shows transcriptomic analyses for more than 45000 genes.

The color codes used in the Excel document are:
Medium or Control - pink
Medium + DMPO - yellow
Medium + LPS - green
Medium + DMPO + LPS - orange

Main conclusions
DMPO by itself causes transcriptomic changes in macrophages.
LPS activate the expression of genes under the transcriptional control of NF-kB
DMPO dampens LPS-induced transcriptomic changes.
Remarkably DMPO activates the expression of genes under the transcriptional control of Nrf2.

These data suggest that DMPO can be a potential structural platform for the design of novel kind of mechanism-based anti-inflammatory, antioxidant and poadipogenic drugs for the treatment of chronic inflammatory diseases, in which the phenotypic switch of macrophages from M2 to M1, is the main pathogenic mechanism.
The use of DMPO to block LPS-induced inflammation cytokine storm in sepsis is considered as a life saving therapeutic strategy.