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Fig. 2 | Molecular Medicine

Fig. 2

From: Elevated AGE-Modified ApoB in Sera of Euglycemic, Normolipidemic Patients with Atherosclerosis: Relationship to Tissue AGEs

Fig. 2

AGE-receptor immunoreactivity in atheromatous human carotid artery

(A) Left: Adhering and infiltrating mononuclear cells within the thickened intima and at the luminal side of the vessel, and carotid endothelium stained for AGE-R1. (magnification × 100) Right: Same as in A left, stained with AGE-R2 antibody, (magnification × 100) (B) Left: Higher magnification (× 200) of an area with intimai thickening and positive staining for AGE-R1 in monocytes, migrating through the endothelium. Right: Corresponding section to that on the left, showing AGE-R2-IR with a similar distribution pattern, but more intensely staining vascular endothelium, (magnification × 200) (C) Left: Section through vasa vasorum within an atheromatous carotid artery, AGE-R1-IR is intense within the smooth muscle cells and endothelium, (magnification × 200) Right: Corresponding section to C left, stained with anti-AGE-R2-antibody shows a similar distribution pattern to AGE-R1. (magnification × 200) (D) Left: Section through an area of dense atheroma of a carotid artery. AGE-R1-IR appears intense within macrophages in the center of the plaque, (magnification × 100) Right: Corresponding section to D left showing AGE-R2 of a similar distribution pattern to that of AGE-R1. (magnification × 100) (E) Left: Section through a recanalizing vessel at the center of a dense carotid plaque. Note AGE-R1-IR in the monocytes/macrophages migrating through the injured vascular endothelium, (magnification × 100) Right: Corresponding section to that on left, AGE-R2 also stained strongly in cells infiltrating recanalizing vessel walls of dense plaques, (magnification × 200)

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