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. 2014 Jun 5;25(11):2459–2470. doi: 10.1681/ASN.2013121307

Figure 6.

Figure 6.

Tcf21 is required in aging podocytes and protects mice from diabetic nephropathy. (A) Upper panel: Long-term follow-up of urinary protein-to-creatinine ratios taken from control and protected podTcf21 mice (defined by protein-to-creatinine ratio<10 mg/mg at 8 weeks of age). PodTcf21 mutants show sporadic mild proteinuria after 32 weeks. Lower panel: Controls and podTcf21 mutants without proteinuria at 17 weeks were rendered diabetic by streptozotocin injection. Diabetic podTcf21 mutants develop massive proteinuria. (B) Representative histologic findings of glomeruli from each group at the end of the study. Aged podTcf21 mutants show mild sclerosis (arrowheads, upper right). Diabetic podTcf21 kidneys show severe glomerulosclerosis and nodular lesions (arrowheads, lower right), while control diabetic mice show mild mesangial expansion only (lower left). Diabetic podTcf21 mice show a significant decrease in survival (C) and increase in occurrence of proteinuria (D). (E) Wild-type diabetic mice show reduced expression of Tcf21 in glomeruli. Bars show mean±SEM. *P<0.05 compared with podTcf21; **P<0.01 compared with podTcf21. DM, diabetes mellitus.