Skip to main content
. 2023 Oct 28;6:1097. doi: 10.1038/s42003-023-05484-9

Fig. 4. CIS-induced acute kidney injury model using chimeric nephrons.

Fig. 4

a A schematic of the CIS-induced acute kidney injury model. b, c Immunostaining images of chimeric nephrons. The expression of kidney injury molecule 1 (Kim1) in proximal tubule cells (PTCs, LTL+) of host (GFP−) and donor (GFP+) origin increases in a CIS dose-dependent manner. d Kim1 positivity of host and donor PTCs (n = 6 sections from 3 biologically independent samples) after CIS treatment. Error bars represent means ± SEM. Data were analyzed using the two-tailed unpaired t-test. ns, not significant. *p < 0.05; **p < 0.01; ****p < 0.0001. e–g Comparisons between the samples at 2 weeks, CIS (−) and 2 weeks, CIS (+) (Fig. 3a) for both host and donor PTCs. e A comparison of the extent of individual gene expression changes upon CIS administration, shown by log2 fold change (log2FC), between host PTCs (n = 1291 cells in 2 weeks, CIS (−) vs. n = 1698 cells in 2 weeks, CIS (+)) and donor PTCs (n = 20 cells in 2 weeks, CIS (−) vs. n = 29 cells in 2 weeks, CIS (+)). f Heatmaps displaying genes with high variability, both up- and downregulated upon CIS administration, in host and donor PTCs. Genes with significant expression changes (log2FC > 1 and p < 0.05) in both host and donor PTCs are highlighted in red (upregulated) and blue (downregulated). g Violin plots showing normalized expression levels of representative variable genes in host and donor PTCs without (blue) and with (orange) CIS treatment. Scale bars, 100 μm in (b) and 20 μm in (c). CIS, cisplatin; DAPI, 4’,6-diamidino-2-phenylindole; GFP, green fluorescent protein; LTL, lotus tetragonolobus lectin.