Skip to main content
. 2023 Jul 3;10(25):2301492. doi: 10.1002/advs.202301492

Figure 1.

Figure 1

External source miR‐186‐5p initiates renal tubular inflammation and tissue injury in the ADR mouse model. A,B) ADR treatment elevated miR‐186‐5p level in A) mouse plasma particularly B) circulating CD8 T cells. C) Depletion of CD8 T cell with anti‐CD8 antibody in ADR mouse decreased miR‐186‐5p level in plasma. D,E) ADR treatment increased the level of D) miR‐186‐5p but not E) pre‐miR‐186‐5p in the mouse kidney. F) Top: Schematic of adenovirus‐based miR‐186‐5p sponge treatment. Bottom: miR‐186‐5p sponge abolished the increase of miR‐186‐5p level in mouse plasma (left) and kidney (right) by ADR treatment. G) Adenovirus‐based miR‐186‐5p sponge attenuated renal tubular injury in ADR mice. H) Flow cytometry analysis of infiltration of macrophages (F4/80+CD11b+) and T cells (CD45+CD3+) in ADR mice with or without miR‐186‐5p sponge treatment. I) Tissue staining of macrophages and CD8 T cells in mouse kidney with or without ADR plus miR‐186‐5p sponge treatment. Scale bars, 50 µm. G,I) There were five mice per group; 6–8 fields were analyzed for each mouse. A—H) Data were analyzed by unpaired two‐sided Student's t‐test. *, p < 0.05 and **, p < 0.01. ns, no significance.