Fig. 5: Downregulated ATG5 expression provoked NF-κB activation. | Cell Death & Disease

Fig. 5: Downregulated ATG5 expression provoked NF-κB activation.

From: ATG5-mediated autophagy suppresses NF-κB signaling to limit epithelial inflammatory response to kidney injury

Fig. 5: Downregulated ATG5 expression provoked NF-κB activation.The alternative text for this image may have been generated using AI.

Animals and treatment were the same as described in Fig. 2. a Representative immunofluorescent staining of p-p65 (red) in kidney sections. Cell nuclei were counterstained with DAPI (blue). Scar bar: 20 μm. b Representative immunoblot analysis of p-p65 and p65 in kidney extracts. β-actin was used as a loading control. c Quantitative data of immunoblot for p-p65 protein in kidney samples from the indicated groups. Data are means ± SEM (n = 6); *P < 0.05 vs. sham; #P < 0.01 vs. obstructed kidney of ATG5+/+ mice. d Primary TECs from ATG5+/+ and ATG5−/− mice were stimulated with 10−6 mmol/L of Ang II for 6 or 24 h. Cell lysates were probed with antibodies against the indicated proteins. e Graphic representation of the relative abundance of p-p65 normalized with β-actin. Data are means ± SEM (n = 3); *P < 0.05 vs. Ang II-untreated corresponding TECs; #P < 0.05 vs. ATG5+/+ TECs treated with Ang II for 24 h. f HK-2 cells were transiently transfected with either scrambled or ATG5 siRNA followed by treatment with Ang II for the indicated time point. Cell lysates were subjected to immunoblot analysis, β-actin was used as a loading control. g Relative expression levels of p-p65 normalized to β-actin. Data are means ± SEM (n = 3); *P < 0.05 vs. corresponding cells without Ang II treatment; #P < 0.05 vs. scrambled siRNA transfected cells with Ang II treatment for 24 h

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