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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Nat Biotechnol. 2015 Nov;33(11):1193–1200. doi: 10.1038/nbt.3392

Figure 6. Modeling kidney development and injury in kidney organoids.

Figure 6

(a) Schematic for kidney development analysis and nephrotoxicity assay. (b) Representative images of immunohistochemistry in structures derived from hESCs treated with DAPT 10 µM from day 14 to 21. n=4. Notch inhibition suppressed proximal tubule formation. Scale bars: 50 µm. (c) Representative immunohistochemistry in structures treated with gentamicin (5 mg/ml) from day 21 to 23 or cisplatin (5 µM) from day 21 to 22. n=6. Scale bars: 50 µm. Gentamicin and cisplatin induced the upregulation of KIM-1, and cisplatin suppressed CDH1 expression. (d) A low magnification image of gentamicin-treated organoids. Scale bar: 100 µm. CDH1: Cadherin-1 (E-cadherin). PODXL: Podocalyxin-like (Podocalyxin). LTL: lotus tetragonolobus lectin. KIM-1: kidney injury molecule-1. (e) Real-time quantitative PCR of KIM-1 in kidney organoids treated with gentamicin at indicated doses. Data is expressed as mean +/− SEM (n=10). (f) Representative immunohistochemistry of organoids treated with cisplatin (5 or 50 µM) from day 23 to 24 (24 hours). n=4. Scale bars: 50 µm.