CD73 alleviates podocytes injury in adriamycin-induced nephrotic syndrome.

Podocyte injury is considered one of the main causes of kidney diseases occurrence and development. We have demonstrated that Ecto-5'-Nucleotidase (CD73) upregulated during podocyte injury, yet its function in podocyte is still unclear. Mouse podocytes cell line (MPC5) were exposed to the adriamycin (ADR, 0.25 μg/ml) to establish the model of podocytes injury, as well as low expression CD73 with lentivirus transfected shRNA. CD73 expression was verified by western blot and immunofluorescence assay. Cytokines (IL-1β, IL-18), apoptosis and apoposis-related protein (Bax, Caspase-3, Desmin) levels were measured using ELISA assay, Flow cytometry and Western blot, respectively. CD73, the cytokines of IL-1β and IL-18, apoptosis rate and the expression of Bax, Caspase-3 and Desmin were significantly increased in ADR group compared with the control group. Moreover, we also successfully constructed a CD73 down-expressed podocytes cell line. However, in comparsion with the ADR group, the cytokines of IL-1β and IL-18, apoptosis rate and the expression of Bax, Caspase-3 and Desmin protein were remarkably lowered in the ADR+CD73 shRNA group. These findings demonstrate that CD73 alleviates podocyte damage by reducing the inflammation and increasing apoptosis.