Fig. 2
From: Bone marrow-derived Ly6C− macrophages promote ischemia-induced chronic kidney disease

In situ replenishment of Ly6C−macrophages compensates for CCR2 deficiency-induced macrophage sparsity in CCR2−/−kidneys during the chronic phase after I/R injury. a Representative images (left) and quantitative analyses (right) for immunofluorescence labeled F4/80 (green) in the WT and CCR2−/− kidneys at d3 and d20 after I/R. b Q-PCR for F4/80 mRNA level during AKI to CKD progression. c Representative images (left) and double-positive analyses (right) for immunofluorescence-labeled F4/80 (green) and Ki67(red) in the WT and CCR2−/− kidneys at d20 after I/R. d Q-PCR for levels of macrophage growth factors CSF1, CSF2, and IL34 in CCR2−/− and WT kidneys from AKI to CKD. e Scheme. cell-sorting approach. f The percentage (left) and number (right) of Ly6C− macrophage analyses by flow cytometry from the whole kidneys in the WT and CCR2−/− mice. g The percentage (left) and number (right) of Ly6C+ macrophage analyses by flow cytometry from the whole kidneys in the WT and CCR2−/− mice. Scale bars, 100 μm. N = 4–6/group. *P < 0.05, **P < 0.01, ***P < 0.001. Values were means±SD. Mø, macrophages