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

Figure 1 β-Arrestin-2 is increased significantly in renal biopsies from patients with diabetic nephropathy and glomerular endothelial cells from mice with diabetic nephropathy. A: Images of immunohistochemical (IHC) staining to detect the expression of β-arrestin-2 in paraffin sections of human renal tissue from normal controls and patients with diabetic nephropathy (DN) (black bars = 10 μm, n = 5); B: Relative mRNA levels of β-arrestin-2 in the renal cortex of DN mice (mean ± SD, ^cP < 0.001 vs control, n = 8); C: The expression of β-arrestin-2 in the renal cortex of DN mice was analyzed by immunoblotting (^cP < 0.001 vs control, n = 8); D: Representative images of IHC staining to detect the expression of β-arrestin-2 in paraffin sections of the kidneys from control and DN mice (red bars = 20 μm, n = 8); E: Detection of β-arrestin-2 expression in glomerular endothelial cells (GENCs) in streptozotocin (STZ)-induced DN mouse model by immunofluorescence double labeling: Endothelin (red, mark protein in GENCs) and β-arrestin-2 (green) (white bars = 50 μm, n = 8); F: Quantifications showing expression of β-arrestin-2 in the kidneys from different groups of mice (^bP < 0.01 vs control, n = 8).