Fig. 4: IL-6 upregulated FasL levels via NF-κBp65 in myeloid cells in PHG.
From: IL-6-driven FasL promotes NF-κBp65/PUMA-mediated apoptosis in portal hypertensive gastropathy
a FasL and NF-κBp65 phosphorylation (NF-κBp-p65, as p-p65), rather than Fas, were induced in primary myeloid cells isolated from PVL-treated mice. β-actin was used as the loading control. n = 6 per group. b The activity of STAT3 and ERK1/2 were detected in primary myeloid cells isolated from SO (sham operation)- and PVL-treated mice. β-actin was used as the loading control. n = 6 per group. c NF-κBp65 deficiency in myeloid cells downregulated the expression of FasL, without affecting the level of IL-6 in the gastric mucosa of PVL mice (brown, × 400, n = 6 per group). d The levels of NF-κBp-p65, NF-κBp65, IκBα, FasL and Fas in the primary myeloid cells dissociated from PVL-treated mice were determined. p65f/f, floxed p65 mice. p65ΔM/ΔM, myeloid cells specific NF-κBp65 deletion mice. β-actin was used as the loading control. n = 6 per group
