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. 2017 May 24;313(3):F767–F780. doi: 10.1152/ajprenal.00683.2016

Fig. 3.

Fig. 3.

mRNA expression levels of MIF-1, MIF-2/D-DT and its target receptors in WT and Mif−/− mice 48 h after I/R injury. A: Mif−/− mice showed minimal MIF-1 expression compared with WT animals. Treatment with MIF-2/D-DT did not affect MIF-1 expression in Mif−/− mice (left: light gray and gray bars). However, Mif−/− mice showed increased MIF-2/D-DT expression compared with WT mice, which was not further stimulated by MIF-2/D-DT treatment (right: light gray and gray bars). B: RNAseq data revealed that WT mice showed robust expression of Cd74, Cd44, Cxcr2, and Cxcr4 in kidney tissue (dark gray bars). Mif−/− mice showed almost complete lack of Cd44 expression but slightly enhanced Cd74 and Cxcr4 expression levels (gray bars). Treatment with MIF-2/D-DT significantly increased Cd44 expression in Mif−/− mice and also enhanced Cd74 and Cxcr4 expression in Mif−/− animals (light gray bars). C: RNAseq analysis showed markedly decreased PCNA and Ki-67 expression levels in Mif−/− mice (gray bars). MIF-2/D-DT treatment enhanced PCNA and Ki-67 expression levels to 80% and 50% of WT levels respectively (light gray bars). D: Western blot assessment of CD74, CXCR4, D-DT, and MIF1 abundance showed similar results compared with RNAseq data. MIF−/− mice showed enhanced abundance of CD74, CXCR4, and D-DT. MIF-2/D-DT treated mice showed increased abundance in CD74 and CXCR4 compared with WT controls. *P < 0.05, **P < 0.01, ***P < 0.001 compared with WT; #P < 0.05, ##P < 0.01; 6–8 animals per experimental group.