Fig. 8: PUMA participated in Fas/FasL/NF-κBp65-mediated epithelial apoptosis in PHG.
From: IL-6-driven FasL promotes NF-κBp65/PUMA-mediated apoptosis in portal hypertensive gastropathy
a Real-time PCR suggested PUMA mRNA expression was increased by fivefold in PHG and fourfold in PVL-treated mice, compared with their control group, respectively. β-actin was used as an internal control. n = 6 in each group, values are presented as mean ± SEM. Bonferroni’s comparison post hoc test. b Immunohistochemical staining of PUMA was presented (brown, upper panel, × 400, n = 6 per group). The levels of PUMA in the indicated tissues were analyzed by western blotting (lower panel). β-actin was used as the loading control. c PUMA staining demonstrated that deletion of NF-κBp65 in myeloid cells of PUMA-WT mice repressed the expression of PUMA (brown, × 400, n = 6 per group). d Western blotting indicated that deletion of NF-κBp65 in myeloid cells of PUMA-WT mice attenuated PUMA-mediated apoptosis (left panel). β-actin was used as the loading control. n = 6 per group. e Immunohistochemical staining showed deletion of PUMA in p65f/f mice attenuated PVL-induced apoptosis (TUNEL staining) without affecting the station of NF-κBp65 activity (p-p65 staining) and Fas level (brown, × 400, n = 6 per group). f, g Western blotting depicted that PUMA deficiency in p65f/f mice suppressed cleaved caspase-3 expression without influencing the levels of Fas, FasL and NF-κBp65 activity in PVL-treated mice. β-actin was used as the loading control. n = 6 per group. h The gastric injury index analysis represented that gastric mucosal injury was attenuated in PVL-treated p65f/f/PUMA-KO mice compared with p65f/f/PUMA-WT mice. n = 6 in each group, values are presented as mean ± SEM. *P < 0.05 versus SO mice, #P < 0.05 versus PVL-treated p65f/f/PUMA-WT mice
