Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Lappas, M. et al.

Lipopolysaccharide and TNF-alpha Activate the Nuclear Factor Kappa B Pathway in the Human Placental JEG-3 Cells.

Up-regulation of pro-inflammatory cytokines, cyclooxygenase ( COX-2) and prostaglandins is a critical factor driving human term labour and inflammation-associated preterm labour. Nuclear factor kappa B (NF-kappaB) is activated in response to a number of inflammatory mediators, including cytokines and lipopolysaccharide (LPS). The aim of this study was (i) to investigate if TNF-alpha and LPS activate the NF-kappaB pathway; and (ii) to use short interfering RNA (siRNA) against inhibitor kappaB kinase (IKK)-beta to confirm the role of the NF-kappaB pathway in the regulation of pro-inflammatory mediators in human placental JEG-3 cells. JEG-3 cells (3 independent experiments) were (i) incubated in the presence or absence of 10mug/ml LPS or 20ng/ml TNF-alpha, or (ii) transfected with 100nM IKK-beta siRNA. Incubation of JEG-3 cells with LPS and TNF-alpha increased the expression of cytoplasmic IKK-beta and phosphorylated IkappaB-alpha, and nuclear NF-kappaB proteins p50 and p65. This was associated with a concurrent increase in COX-2 protein, and IL-6 and PGF(2alpha) release from JEG-3 cells. Treatment of cells with BAY 11-7082 at 50muM significantly inhibited basal, LPS- and TNF-alpha- induced NF-kappaB and COX-2 expression, and IL-6 and PGF(2alpha) release. Transfection of JEG-3 cells with IKK-beta siRNA significantly decreased IL-6 and PGF(2alpha) release. The data presented in this study demonstrate that pro-inflammatory mediators regulate the NF-kappaB transcription pathway in human JEG-3 cells, and the IKK-beta/NF-kappaB pathway is a regulator of inflammatory mediators in placental JEG-3 cells.[1]

References

Lipopolysaccharide and TNF-alpha Activate the Nuclear Factor Kappa B Pathway in the Human Placental JEG-3 Cells. Lappas, M., Yee, K., Permezel, M., Rice, G.E. Placenta (2006) [Pubmed]

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