Figure 1.
Figure 1. CCR5 but not CCR1 deficiency inhibits neointima formation: role of IL-10. (A) Carotid arteries of CCR5+/+apoE–/– and CCR5–/–apoE–/– mice, CCR1+/+apoE–/– and CCR1–/–apoE–/– mice after wire injury. Representative sections stained with pentachrome (scale bars represent 100 μm) and quantification of neointimal areas (right panels, *P < .05) are shown. ○ represents individual mice; ♦, mean ± SEM. (B) Quantification of macrophage content in injured carotid arteries of CCR5+/+apoE–/– and CCR5–/–apoE–/– mice treated with or without blocking IL-10 mAb, and of CCR1+/+apoE–/– and CCR1–/–apoE–/– mice treated with or without blocking IFN-γ mAb (*P < .05). Error bars indicate SEM. (C) Immunofluorescence staining for CCR2 (nuclear DAPI staining as inserts) and (D) SMCs and IL-10 in CCR5+/+apoE–/– mice and CCR5–/–apoE–/– mice (scale bars represent 25 μm).

CCR5 but not CCR1 deficiency inhibits neointima formation: role of IL-10. (A) Carotid arteries of CCR5+/+apoE–/– and CCR5–/–apoE–/– mice, CCR1+/+apoE–/– and CCR1–/–apoE–/– mice after wire injury. Representative sections stained with pentachrome (scale bars represent 100 μm) and quantification of neointimal areas (right panels, *P < .05) are shown. ○ represents individual mice; ♦, mean ± SEM. (B) Quantification of macrophage content in injured carotid arteries of CCR5+/+apoE–/– and CCR5–/–apoE–/– mice treated with or without blocking IL-10 mAb, and of CCR1+/+apoE–/– and CCR1–/–apoE–/– mice treated with or without blocking IFN-γ mAb (*P < .05). Error bars indicate SEM. (C) Immunofluorescence staining for CCR2 (nuclear DAPI staining as inserts) and (D) SMCs and IL-10 in CCR5+/+apoE–/– mice and CCR5–/–apoE–/– mice (scale bars represent 25 μm).

Close Modal
This Feature Is Available To Subscribers Only

or Create an Account

Close Modal
Close Modal