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

Figure 3 Knockdown of β-arrestin-2 by siRNA ameliorates high glucose induced glomerular endothelial cell injury and apoptosis. A: Images showing efficiency of silencing β-arrestin-2 with small interfering RNA (siRNA) by Western blotting (^aP < 0.05 vs control, n = 6); B: Representative images showing effect of β-arrestin-2 knockdown on expression of occludin, ZO-1, and eNOS in high glucose (HG)-treated glomerular endothelial cell (GENCs) by Western blotting (^bP < 0.01 vs scramble/control, ^dP < 0.05 vs scramble/HG treatment, n = 6); C: Immunoblotting images showing effect of β-arrestin-2 knockdown on expression of apoptosis related proteins Bcl-2 and Bax in HG-treated GENCs (^aP < 0.05 vs scramble/control, ^cP < 0.001 vs scramble/control, ^dP < 0.05 vs scramble/HG treatment, n = 6); D: Immunoblotting images showing effect of β-arrestin-2 knockdown on expression of cleaved caspase 3 and caspase 3 in GENCs with HG treatment (^cP < 0.001 vs scramble/control, ^eP < 0.01 vs scramble/HG treatment, n = 6); E: Flow cytometric images showing decreased apoptosis of GENCs with HG treatment by knockdown of β-arrestin-2; F: Summarized flow cytometric data showing reduced apoptosis of GENCs with HG treatment by silencing β-arrestin-2 (^bP < 0.01 vs scramble/control, ^dP < 0.05 vs scramble/HG treatment, n = 6). HG: High glucose; siRNA: Small interfering RNA.