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. 2022 Dec 5;13:7497. doi: 10.1038/s41467-022-35306-1

Fig. 7. Deletion of Il11ra1 in tubular epithelial cells protects against acute kidney injury.

Fig. 7

a Schematic of induction of AKI injury in Cadh16-Cre+/- Il11ra1loxP/loxP mice for experiments shown in (b–i). Cadh16-Cre+/- Il11ra1loxP/loxP and littermate control (Cadh16-Cre−/− Il11ra1loxP/loxP) mice were injected intraperitoneally with 200 mg/kg FA. Blood and kidneys were collected on day 28 post FA. b Western blots showing renal expression of IL11, pERK, ERK, pp90RSK, p90RSK, pGSK3β, GSK3β, SNAI1, ZEB, E-Cadherin, Cyclin D1, αSMA, Fibronectin (FN1), and GAPDH (representative dataset from n = 5/group, except for WT-NaHCO3: n = 4), c kidney weights, d kidney collagen content by hydroxyproline assay, e representative Masson’s Trichrome images of whole kidney cross section (scale bars: 500 µm, representative dataset from n = 5/group, except for WT-NaHCO3: n = 4), f quantification of collagen area from Masson’s Trichrome-stained kidney sections (n = 5/group, except for WT-NaHCO3: n = 4), g BUN, h serum creatinine, i urine ACRs, j heatmaps showing renal mRNA expression of fibrotic markers (Col1a1, Col1a2, Col3a1, Fn1, Acta2), pro-inflammatory markers (Tnfα, Il6, Ccl2, Ccl5, Il1β), kidney injury markers (Ngal, Kim1), and pEMT markers (Snai1, Zeb) (values are shown in Supplementary Fig. 10). c, d, g–i WT-NaHCO3 (n = 4), CKO-NaHCO3 (n = 5), WT-FA (n = 8), CKO-FA (n = 7). c, d, f–i Data are shown as box-and-whisker with median (middle line), 25th–75th percentiles (box), and minimum–maximum values (whiskers); two-way ANOVA with Sidak’s correction. Source data are provided as a Source data file.