FIGURE 1.

Expression and activity of HDAC6 in podocytes of type 2 diabetic patients, db/db mice and AGE‐treated podocytes. Representative fluorescence (A), quantification of HDAC6 (B) and activity of HDAC6 were determined in the kidneys of healthy controls and DN patients (C, n = 6). The mRNA level of HDAC6 in the kidneys of healthy controls and DN patients (D, n = 7). Positive correlation of HDAC6 mRNA levels with Scr (E) and negative correlation with eGFR (F) in all subjects. The mRNA (G) and activity (H) level of HDAC6 in the kidneys of db/m and db/db mice (n = 5). Cultured podocytes were treated with AGE for the indicated time (I). Summarized data indicated that AGE inhibited LC3‐II and Beclin‐1 expression at 72 h (I). Representative Western blot of HDAC6 (J) and densitometric analyses of the HDAC6 activity in podocytes following AGE treatment (K). At least 3 times repeat for each experiment in vitro. AGE, advanced glycation end products; BSA, bovine serum albumin; CON, control; DN, diabetic nephropathy; eGFR, estimated glomerular filtration rate; HDAC6, histone deacetylase 6; MFI, mean fluorescence intensity; PBS, phosphate buffer saline; Scr, serum creatinine