β-Arrestin-2 enhances endoplasmic reticulum stress-induced glomerular endothelial cell injury by activating transcription factor 6 in diabetic nephropathy

Figure 4 Knockdown of β-arrestin-2 reduces endoplasmic reticulum stress and apoptosis of glomerular endothelial cells in high glucose treatments by decreasing expression of activating transcription factor 6. A: Representative images and summarized data showing that knockdown of β-arrestin-2 inactivated endoplasmic reticulum (ER) stress by downregulating expression of BiP and CHOP in HG-treated glomerular endothelial cells (GENCs) by Western blotting (^aP < 0.05 vs scramble/control, ^bP < 0.01 vs scramble/control, ^dP < 0.05 vs scramble/HG treatment, n = 6); B: Flow cytometric analysis showing that the ER stress activators tunicamycin (TM) and thapsigargin (TG) induced GENC apoptosis and the inhibitor 4-phenyl butyric acid (4-PBA) reduced GENC apoptosis (^bP < 0.01 vs scramble/control, ^fP < 0.05 vs TM/TG treatment, n = 5); C: Summarized flow cytometric data showing apoptosis of GENCs under different stimuli (^aP < 0.05 vs scramble/control, ^bP < 0.01 vs scramble/control, ^dP < 0.05 vs scramble/HG treatment, ^fP < 0.05 vs TM/TG treatment, n = 4); D: Western blotting images showing effects of β-arrestin-2 knockdown on expression of ATF6 in GENCs under HG treatment (^bP < 0.01 vs scramble/control, ^dP < 0.05 vs scramble/HG treatment, n = 6). HG: High glucose; siRNA: Small interfering RNA; TM: Tunicamycin; TG: Thapsigargin; 4-PBA: 4-Phenyl butyric acid.