Research Paper Volume 11, Issue 6 pp 1804—1820

Endothelial cells secreted endothelin-1 augments diabetic nephropathy via inducing extracellular matrix accumulation of mesangial cells in ETBR-/- mice

Figure 5. ET-1 promoted RhoA/ROCK pathway in mesangial cells through ETAR. Mesangial cells were treated with 1 nM ET-1, ABT-627(25μM, inhibitor of ETAR pathway) or A192621 (25μM, inhibitor of ETBR pathway) for 24 h. (A-C) Mesangial cell proliferation, RhoA/ROCK and ECM-related proteins, and cell apoptosis were detected in control, ABT-627, A192621, ET-1, ET-1+ ABT-627, ET-1+A192621 groups. **p<0.01 compared with ET-1 group. (D) Expression quantity from gene transcription level of EDNRA and EDNRB in mouse mesangial cells SV40 MSE 13 and mouse primary mesangial cells. **p<0.01 compared with ETAR. (E) ETAR and ETBR expressions on mesangial cell membrane were measured in ET-1 treated SV40 MSE 13 cells and primary mesangial cells. Bars depict the mean ± SD. N=3.