Fig. 4.
CCR2−/− mice do not show increased numbers of cardiac macrophages and cardiac dysfunction during chronic kidney disease. A F4/80+MHCIIhi and F4/80+MHCIIlo resident macrophage numbers per mg of heart tissue in vehicle and folate treated (wild-type) WT and CCR2−/− mice (* P < 0.05). B Ejection fraction (left) and fractional shortening (right) measured by echography in vehicle and folate treated WT and CCR2−/− mice (* P < 0.05). C Cardiac levels of troponin I in ng/mL in vehicle and folate treated WT and CCR2−/− mice. D Intracarotid mean, systolic (SBP) and diastolic (DBP) blood pressure expressed in mmHg in vehicle and folate treated WT and CCR2−/− mice. E Fold change from vehicle in expression of extracellular matrix and cardiac injury genes in folate treated WT and CCR2−/− mice. Grey line represents no change from control (* P < 0.05, ** P < 0.01). F Cardiomyocyte cell areas and geodesic diameters (length of the shortest path between two furthest points) in hearts of vehicle and folate treated WT and CCR2−/− mice. Each point represents the mean of at least 1000 to 3000 cardiomyocytes per animal (** P < 0.01, *** P < 0.001)