Fig. 4
From: ATG5 and ATG7 induced autophagy interplays with UPR via PERK signaling
Determination the effect of ATG5 and ATG7 on autophagy flux. a The C28I2 cells were treated with Rapamycin (25 μM), pcDNA3.1(−), pcDNA3.1(−)-ATG5, pcDNA3.1(−)-ATG7, pcDNA3.1(−)-ATG5 + pcDNA3.1(−)-ATG7, Bafilomycin A1(0.4 μM), and Bafilomycin A1(0.4 μM) + pcDNA3.1 (−)-ATG5 + pcDNA3.1(−)-ATG7, then immediately stained with the anti-LC3 antibody, anti-LAMP1 antibody and DAPI respectively, and visualized by confocal microscopy (400×). b Transmission electron microscopy (TEM) analysis showing autophagosome (arrowed) after treated with Rapamycin (25 μM), Ad-GFP, Ad-ATG5, Ad-ATG7 and Ad-ATG5 + Ad-ATG7 for 24 h in the C28I2 cells. The autophagosome is shown by red arrow. Rapamycin (25 μM) used as a positive control, Bafilomycin A1 is a lysosomal inhibitor. c Qualitative analysis of LC3 and LAMP1 fluorescence intensity of chondrocytes under confocal microscopy. The values were normalized to the NC group. d Qualitative analysis of the number of autophagosome in chondrocytes under TEM. The values were normalized to the NC group