Transmembrane redox signaling activates NF-kappaB in macrophages.
In macrophages, NF-kappaB can be activated by H2O2 generated by the respiratory burst or added exogenously. The mechanism of H2O2 signaling may involve changes in the cellular redox state or a redox reaction at the plasma membrane; however, the site of H2O2 action cannot be readily ascertained because of its membrane permeability. Ferricyanide, a nonpermeable redox active anion, activated NF-kappaB in the macrophage cell line, J774A.1. In contrast with exogenous H2O2, activation by ferricyanide did not correlate with net oxidation of NAD(P)H or glutathione, suggesting that a transplasma membrane redox reaction itself was the first signaling process in NF-kappaB activation.
Kaul
N
N
Department of Molecular Pharmacology & Toxicology, University of Southern California, Los Angeles 90033, USA.
Choi
J
J
Forman
H J
HJ
D000818:Animals; D002460:Cell Line; D002463:Cell Membrane Permeability; D006861:Hydrogen Peroxide / Q000378:metabolism*; D008264:Macrophages / Q000378:metabolism*; D051379:Mice; D009249:NADP / Q000032:analysis; D016328:NF-kappa B / Q000378:metabolism*; D010084:Oxidation-Reduction; D016897:Respiratory Burst / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*; D013050:Spectrometry, Fluorescence
D016328:NF-kappa B; D009249:NADP; D006861:Hydrogen Peroxide