IndraLab

"Although molecular interactions between TNF-alpha and PGE2 are largely unexplored in human malaria, results presented here show that pfHz induced suppression of PBMC COX-2 gene products induces overproduction of TNF-alpha."

"The major findings of this study are: first, LPS, TNF-α, and PGE2 associate with their receptors such as TNFR/TLR and EP receptors to trigger the RGS12 expression; second, the increased RGS12 promotes the phosphorylation of NF-κB and IκB, IκB proteolysis, and nuclear translocation of NF-κB; third, deletion or silence of RGS12 in macrophages inhibits the release of pro-inflammatory cytokines in RA, through the reduced activation of NF-κB(p65); fourth, PTB domain promotes the association of RGS12 and NF-κB(p65), and NF-κB(p65) inversely regulates the transcription of the RGS12 gene, which forms an auto-regulatory feedback loop; last but not least, COX2 enhances nuclear translocation of RGS12/NF-κB(p65) in inflammatory conditions."

"As expected, the EP2-R agonist failed to inhibit TNFα-production in EP2-R-deficient cells while the EP4-R agonist did not attenuate TNFα-formation in EP4-R-deficient cells ( Fig. 2 )."