Figure 7
Figure 7. IKK-β inhibition has no effect on the hypoxic induction of various genes in human MDMs in vitro: use of a recombinant adenovirus expressing a dominant negative inhibitor of IKK-β (adv-IKK-βDN). MDM infection with adv-IKK-βDN (but not control adv) significantly inhibited both TNF-α–induced gene expression of CXCL8 (A) and hypoxia-induced nuclear accumulation of phospho-p65/RelA (B) by human MDM. (C) Hypoxia significantly increased the expression of VEGFA, CXCL8, CXCR4, GLUT-1, and ADM mRNA in untreated and adenovirally infected MDM compared with respective normoxic MDM controls. However, there was no significant difference in the expression of these genes between hypoxic MDM infected with adv-IKK-βDN or the control adenovirus. N = 3. *P < .05 with respect to respective normoxic group. +P < .05 with respect to TNF-α + control adenovirus group.

IKK-β inhibition has no effect on the hypoxic induction of various genes in human MDMs in vitro: use of a recombinant adenovirus expressing a dominant negative inhibitor of IKK-β (adv-IKK-βDN). MDM infection with adv-IKK-βDN (but not control adv) significantly inhibited both TNF-α–induced gene expression of CXCL8 (A) and hypoxia-induced nuclear accumulation of phospho-p65/RelA (B) by human MDM. (C) Hypoxia significantly increased the expression of VEGFA, CXCL8, CXCR4, GLUT-1, and ADM mRNA in untreated and adenovirally infected MDM compared with respective normoxic MDM controls. However, there was no significant difference in the expression of these genes between hypoxic MDM infected with adv-IKK-βDN or the control adenovirus. N = 3. *P < .05 with respect to respective normoxic group. +P < .05 with respect to TNF-α + control adenovirus group.

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