Heme Oxygenase-1-derived Carbon Monoxide Requires the Activation of Transcription Factor NF-κB to Protect Endothelial Cells from Tumor Necrosis Factor-α-mediated Apoptosis

We have shown that carbon monoxide (CO) generated by heme oxygenase-1 (HO-1) protects endothelial cells (EC) from tumor necrosis α (TNF-α)-mediated apoptosis. This effect relies on the activation of p38 MAPK. We now demonstrate that HO-1/CO requires the activation of the transcription factor NF-κB to exert this anti-apoptotic effect. Our data suggest that EC have basal levels of NF-κB activity that sustain the expression of NF-κB-dependent...