Fig. 3
From: ATG5 and ATG7 induced autophagy interplays with UPR via PERK signaling
ATG5 and ATG7 enhanced autophagy and inhibited ER stress in chondrocyte. a Western blotting analysis of LC3, P62, ATG5, ATG7 and ATG5-ATG12 expression after infected with Ad-ATG5, Ad-ATG7 and Ad-ATG5 + Ad-ATG7 in the C28I2 cells. β-actin is served as an internal control. b Qualitative analysis of ATG5, ATG7, ATG5-ATG12, LC3 and P62. The values were normalized to β-actin. c C28I2 cells were double stained with LC3 (red) and DAPI (blue) and visualized by confocal microscopy (400X) after treated with Rapamycine, Ad-ATG5, Ad-ATG7 and Ad-ATG5 + Ad-ATG7 24 h. *P < 0.05, **P < 0.01 compared with the controls. Values are means ± SD n = 3). d Qualitative analysis of LC3 fluorescence intensity of chondrocytes. The values were normalized to the NC group. e Western blotting analysis of PERK, p-PERK and Nrf2 expression after infected with Ad-ATG5, Ad-ATG7 and Ad-ATG5 + Ad-ATG7 in the C28I2 cells. β-actin is served as an internal control. f Qualitative analysis of PERK, p-PERK and Nrf2 were normalized to β-actin. (1:NC, 2:Ad-GFP, 3:Ad-ATG5, 4:RAPA, 5:Ad-ATG7, 6:Ad-ATG5 + RAPA, 7:Ad-ATG5 + Ad-ATG7). Rapamycin (25 μM) used as a positive control