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. 2014 Apr 17;7(6):701–710. doi: 10.1242/dmm.014548

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© 2014. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 2. — Delayed HOE-140 treatment protects mice from the development of FSGS. At day 7 after treatment with 10 mg of Adriamycin (ADM) per kg of bodyweight, balb/c mice were killed. Treatment with HOE-140 protected mice from proteinuria (A) and albuminuria (B). HOE-140 also prevented the downregulation of the mRNAs that encode the podocyte proteins nephrin (NPHS-1) (C), and WT-1 (F), although the treatment showed no difference in podocin (NPHS-2) (D) and α-actinin-4 (ACTN-4) (E) between groups. Expression of the mRNAs were normalized to that of hypoxanthine guanine phosphoribosyl transferase (HPRT). (G) We observed, by using electron microscopy analysis, that HOE-140 prevented the podocyte foot process effacement that was induced by ADM injection. The black arrow indicates podocyte effacement. *P<0.05 compared with that of control mice, ^#P<0.05 compared with that of mice treated with only ADM. Five animals were used per study group.