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

Figure 5 Overexpression of β-Arrestin-2 aggravates glomerular endothelial cell injury and apoptosis by activating endoplasmic reticulum stress through upregulation of activating transcription factor 6. A: Representative images showing that overexpression of β-arrestin-2 enhanced expression of BiP and CHOP in glomerular endothelial cells (GENCs), which could be blocked by knockdown of activating transcription factor 6 (ATF6) (^aP < 0.05 vs scramble/control, ^gP < 0.05 vs pCDNA-β-arrestin-2 treatment, n = 6); B: Representative images showing that overexpression of β-arrestin-2 reduced expression of ZO-1 and Occludin in GENCs, which could be recovered by knockdown of ATF6 in GENCs (^aP < 0.05 vs scramble/control, ^bP < 0.01 vs scramble/control, ^hP < 0.01 vs pCDNA-β-arrestin-2 treatment, n = 6); C: Representative images showing that overexpression of β-arrestin-2 promoted apoptosis related protein expression in GENCs, which was blocked by knockdown of ATF6 (^aP < 0.05 vs scramble/control, ^bP < 0.01 vs scramble/control, ^gP < 0.05 vs pCDNA-β-arrestin-2 treatment, n = 6); D: Summarized flow cytometric data showing that overexpression of β-arrestin-2 aggravated apoptosis of GENCs, which was inhibited by knockdown of ATF6 (^aP < 0.05 vs scramble/control, ^gP < 0.05 vs pCDNA-β-arrestin-2 treatment, n = 6); E: Representative Western blot images showing that overexpression of β-arrestin-2 upregulated expression of ATF6, but knockdown of ATF6 did not affect expression of β-arrestin-2 (^aP < 0.05 vs scramble/control, ^bP < 0.01 vs scramble/control, ^gP < 0.05 vs pCDNA-β-arrestin-2 treatment, n = 6). ATF6: Activating transcription factor 6.