[HTML][HTML] Heme oxygenase-1-derived carbon monoxide requires the activation of transcription factor NF-κB to protect endothelial cells from tumor necrosis factor-α …
S Brouard, PO Berberat, E Tobiasch, MP Seldon… - Journal of Biological …, 2002 - ASBMB
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
anti-apoptotic genes required to support the anti-apoptotic effect of HO-1/CO. Over …
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
anti-apoptotic genes required to support the anti-apoptotic effect of HO-1/CO. Over …