Fig. 6

HSA-treated tubular epithelial cell-derived EVs promoted macrophage glycolysis by stabilizing HIF-1α. A Double IHC staining of HIF-1α (red) and F4/80 (green) in the kidney cortexes of db/m and db/db mice. Macrophages were co-cultured with tubular epithelial cell-derived EVs: B, C protein level of HIF-1α and extent of HIF-1α hydroxylation (n = 3); *p < 0.05 vs. the Control-HK-2-EVs group; ^#p < 0.05 vs. the Control-HK-2-EVs + LPS group; D double IHC staining of HIF-1α (red) and F4/80 (green) in the kidney cortexes of db/db + Control-HK-2-EVs and db/db + HSA-HK-2-EVs mice. Macrophages transfected with HIF-1α siRNA and co-cultured with HSA-HK-2-EVs: E mRNA levels of GLUT1, HK2, LDHA, IL1β and TGF-β1 (n = 3); F, G protein levels of HK2 and LDHA (n = 4); H amount of lactate in the macrophage supernatant (n = 3); *p < 0.05 vs. the Si-NC + HSA-HK-2-EVs + LPS group. MiRNAs and lncRNAs that have been reported to modulate HIF-1α expression were measured in EVs. *p < 0.05 vs. the Control-HK-2-EVs group (n = 3)