Fig. 3: ATG5 deletion in TECs increases IL-1β production.
Animals and their treatment were the same as described in Fig. 2. a Representative immunofluorescence staining of IL-1β (red) in kidney sections. Scar bar: 20 μm. Cell nuclei were counterstained with DAPI (blue). b Representative images of immunoblot analysis of pro-IL-1β, cleaved IL-1β, LC3, ATG12–ATG5 kidney extracts. β-actin was used as a loading control. c Quantitative data of immunoblot for pro-IL-1β protein in kidney samples from the indicated groups of mice. Data are means ± SEM (n = 6); *P < 0.05 vs. sham; #P < 0.01 vs. obstructed kidney of ATG5+/+ mice. d HK-2 cells were treated with 10−6 mmol/L of Ang II for the indicated time point. Cell lysates were subjected to immunoblot analysis for pro-IL-1β, cleaved IL-1β, and LC3. β-actin was used as a loading control. e Pro-IL-1β and LC3 contents were quantitatively analyzed using a densitometer. Values are mean ± SEM (n = 3); *P < 0.01 vs. control group. f Primary TECs from ATG5+/+ and ATG5−/− mice were stimulated with 10−6 mmol/L of Ang II for 24 or 48 h. Cell lysates were probed with antibodies against the indicated proteins. g Densitometry of pro-IL-1β in immunoblots. Data are means ± SEM (n = 3); *P < 0.05 vs. respective control; #P < 0.05 vs. cells from ATG5+/+ TECs treated with Ang II for 48 h
