Fig. 5
Phagocytosis was associated with venogenesis in the infarct core. (A) Transmission electron microscopy images of the infarct core on day 10. (a1) Foamy macrophages in the infarct region. (a2) Magnification of lipid-rich foamy macrophages. (a3) Macrophage engulf cell debris. (a4) A microvessel was spatially close to macrophages. ly, lysosome; lp, lipid droplets; N, nucleus; MCH, macrophage; ECs, endothelial cells; BL, basal lamina; P, pericytes. (B) GIAO staining revealed lipid-rich foamy macrophages and newly formed venules in the infarct core. (C) The top 20 upregulated phagocytosis-associated genes (fold change ≥ 2 and p < 0.05) in the infarct core (n = 5). (D) mRNA expression of macrophage markers of different phenotypes on day 10. n = 4. *p < 0.05 vs. control. ※p < 0.05 vs. peri. (E) Immunofluorescence images of CD68-, Arg1-, and Cd206-labeled macrophages in the infarct core on days 3 and 7. Scale bar, 50 μm. (F) ALP staining of microvessels and EPCs in the cortex. (f1) Arterioles in the normal cortex. (f2) and (f3) ALP-labeled EPCs in the infarct region of control mice. (f4) ~ (f6) ALP-labeled EPCs in mice with macrophage depletion (mac-/-). EPCs proliferate and form microvessels from the outer edge of the infarct cortex. (G) Representative CD31-labeled microvessels in the infarct cores of control and mac-/- mice. (H) and (I) Quantitative analysis revealed increased vessel density (ALP, p < 0.0001; CD31, p = 0.006) in mac-/- mice compared with control mice. *p < 0.05