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. 2014 Oct 31;4(1):91–96. doi: 10.1038/kisup.2014.17

Figure 1.

Figure 1

Sustained expression of the Notch1 intracellular domain is sufficient to cause tubulointerstitial fibrosis and glomerulosclerosis. (a) Pax8rtTA animals express the reverse tetracycline transactivator under the Pax8 (tubule epithelial cell specific) promoter. Animals were crossed with tetracycline-inducible (tet-o) NICD1 mice (Pax8rtTA/NICD1, schematic far left panel). Upon doxycycline (dox) administration animals express the Notch intracellular domain in tubule epithelial cells. From left to right micrographs are representative of periodic acid–Schiff (PAS)-stained sections from: wild type (WT), Pax8rtTA with dox, and Pax8rtTA/NICD with dox-fed mice harvested at day 28 post induction. Note the significant tubulointerstitial fibrosis in double-transgenic mice after dox treatment. (b) Tet-o-NICD1 mice were crossed with podocin rtTA animals for podocyte-specific expression of Notch1 (podocin rtTA/NICD1, schematic far left panel). From left to right, micrographs are representative PAS-stained sections from: WT, dox-treated podocin rtTA, and dox-treated podocin rtTa/NICD mice harvested at day 10 post induction. Note the significant glomerulosclerosis and proteinaceous casts. Scale bar=10 μm.