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. 2023 Aug 2;31(10):3067–3083. doi: 10.1016/j.ymthe.2023.07.024

Figure 2.

Figure 2

MSC treatment inhibited TEC inflammation and transdifferentiation

(A) Subclustering of TECs from sham-, IRI-AKI-, and MSC-treated kidneys. (B) Expression of the top 15 DEGs in the TEC subclusters. (C) Expression of representative marker genes in the TEC subclusters. (D) Relative cell percentage distribution and enrichment in the treatment groups. (E) Violin plots showing pathway enrichment in the TEC subclusters, estimated by GSVA. (F) Western blotting showing the levels of KIM-1, TGF-β1, pi-NF-κB, caspase-3, and p53 proteins in IRI-AKI- and MSC-treated kidneys. (G) Multiplex immunostaining in kidney sections showing the expression of fibrotic markers α-SMA (green) and vimentin (red) in IRI-AKI (d 3)- and MSC-treated kidneys. (H) Representative electron microscopic images showing changes in mitochondrial morphology in sham-, IRI-AKI (d 3)-, and MSC-treated kidneys.