Skip to main content
. 2021 Dec 22;43(8):2081–2093. doi: 10.1038/s41401-021-00833-y

Fig. 4. 11R-VIVIT inhibits the nuclear localization and dephosphorylation of NFAT2 in RTECs in an AKI-to-CKD progression model.

Fig. 4

a Double immunofluorescence staining of NFAT2 (green) and DAPI (blue) and merged images of kidneys from the sham-operated, IRI and IRI + 11R-VIVIT treatment groups. Scale bars = 20 μm. b Quantification of the percentage of renal tubular epithelial cells with NFAT2 expression in the nucleus. *P < 0.05 vs. IRI-2d, #P < 0.05 vs. IRI-14d, &P < 0.05 vs. IRI-28d. c Protein expression of p-NFAT2 (Ser172) in the sham-operated, IRI and IRI + 11R-VIVIT treatment groups on the 2nd, 14th and 28th day. d The quantitative results of p-NFAT2 (Ser172) were normalized to GAPDH. NFAT2 nuclear factor of activated T cells 2, RTECs renal tubular epithelial cells, AKI acute kidney injury, CKD chronic kidney disease, IRI ischemia-reperfusion injury, p-NFAT2 phosphorylated nuclear factor of activated T cells 2.