Improvement of membranous nephropathy by inhibition of miR‐193a to affect podocytosis via targeting WT1

The objective of this paper was to explore the role and molecular mechanism of miR‐193a in membranous nephropathy (MN). Experimental rats and podocytes were randomly divided into four groups: control, MN, miR‐NC, and miR‐193a inhibitor groups. The relative mRNA level of miR‐193a was determined. The mRNA level and protein expression of PODXL, NPHS1, and Notch1 were determined by real‐time polymerase chain reaction (RT‐PCR) and Western blot analysis, respectively. The mRNA level and protein expression of WT1 in podocytes were also determined by RT‐PCR and Western blot analysis. The relative mRNA level of miR‐193a in the MN group was significantly higher than that in the control group, and inhibition of miR‐193a inhibited the increase successfully. Inhibition of miR‐193a inhibited renal injury, podocyte injury, and tissue cell apoptosis resulting from MN. The expression of PODXL, NPHS1, and Notch1 was decreased in the MN group, while the expression was increased in the miR‐193a inhibitor group. WT1 was verified as a target gene of miR‐193a and the expression of WT1 increased after inhibition of miR‐193a. Inhibition of miR‐193a by targeting WT1 could inhibit renal function injury, renal tissue cell apoptosis, and podocytosis. Inhibition of miR‐193a could inhibit renal function injury, renal tissue cell apoptosis, and podocytosis by targeting WT1.