Figure 5.

Macrophage MR (mineralocorticoid receptor) deficiency is associated with enhanced neutrophil efferocytosis, suppression of free radical formation and the modulation of fibroblast activation. A, Quantitative reverse-transcriptase polymerase chain reaction was used to detect the relative gene expression of Mertk, C1qa, C1qb, Gpnmb, Cat, Pxdr4, ApoE, Vegfb, IGF1, and Lcn2. B, Phagocytic index for apoptotic neutrophils and (C) phagocytic capacity for zymosan particles of macrophages (CD [cluster of differentiation] 45⁺/CD11b⁺/Ly6G⁻/F4/80⁺ cells) isolated by cell sorting from MR^flox and MR^LysMCre infarcts, 3 d after coronary artery ligation. D, Superoxide production by CD45⁺/CD11b⁺/Ly6G⁻/F4/80⁺ macrophages fluorescence-activated cell sorting–isolated from MR^flox and MR^LysMCre infarcts, assessed using a highly sensitive isocratic ion-pair high performance liquid chromatography–electrochemical method. E, Immunocytochemical staining showing fibroblasts and differentiated α-SMA (α-smooth muscle actin)–positive myofibroblasts (vimentin, red; α-SMA, green) and zymography of conditioned media. Macrophages (CD45⁺/CD11b⁺/Ly6G⁻/F4/80⁺ cells) and fibroblasts (CD45⁻/CD11b⁻/CD31⁻/TER-119⁻/NG2⁻/MEFSK4⁺ cells) were isolated by cell sorting from the infarct myocardium of MR^flox and MR^LysMCre mice and cocultured using the Boyden chamber system. Mean±SEM (n=4–5). MMP indicates matrix metalloproteinase. *P<0.05 vs MR^flox. HE indicates hydroethidine; IS, internal standard; NG2, chondroitin sulfate proteoglycan; MEFSK4, anti-feeder antibody, clone mEF-SK4; and SSC, side scatter.