[No authors listed]
As a member of the cysteine protease family, cathepsin S (CTSS) serves an important role in diseases such as cancer, arthritis and atherosclerosis. Nevertheless, its role in renal fibrosis is unknown. In the present study, the effects of CTSS on renal fibrosis in mild (group M) and severe (group S) hydronephrosis were studied by reverse transcriptionâ-quantitative PCR (RTâqPCR), western blot analysis (WB), Masson's trichrome staining and immunohistochemical staining in mouse models. The effects of CTSS on extracellular matrix (ECM) deposition and epithelialâmesenchymal transition (EMT) and the potential mechanisms were further studied by RTâqPCR and WB in transforming growth factor (TGFâβ1)âstimulated TCMKâ1 cells. Compared with group N (no hydronephrosis), the expression levels of CTSS in the M and S groups were significantly higher, and a significant increase in ECM deposition was observed in the S group. In addition, compared with group N, the expression levels of TGFâβ1, αâsmooth muscle actin (αâSMA), SMAD2, SMAD3, phosphorylated (p)SMAD2 and pSMAD3 in groups M and S were significantly higher, whereas the expression of Eâcadherin was significantly lower. Inhibition of CTSS expression increased the expression levels of TGFâβ1, αâSMA, fibronectin, collagenâI, SMAD2, SMAD3, pSMAD2 and pSMAD3, whereas Eâcadherin expression decreased. A significant increase in CTSS was observed in the TGFâβ1âstimulated TCMKâ1 cell line. ECM deposition and EMT were also intensified. The opposite outcomes occurred after intervention with small interfering RNA targeting CTSS. In conclusion, CTSS affected EMT and the deposition of ECM. CTSS may mediate the regulation of fibrosis by the TGFâβ/SMAD signaling pathway. CTSS may serve an important role in the treatment of renal fibrosis.
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