Inactivation of Semicarbazide-Sensitive Amine Oxidase Stabilizes the Established Atherosclerotic Lesions via Inducing the Phenotypic Switch of Smooth Muscle Cells
Fig 1
SSAO inactivation stabilized the established atherosclerotic lesions under hypercholesterolemia.
Female LDLr KO mice were fed WTD for 6 weeks to induce the formation of atherosclerotic lesions. Thereafter, 0.125% semicarbazide were added in drinking water to inactivate SSAO during the subsequent 3 weeks (A) before the analysis of SSAO activities in the visceral adipose tissue (B), plasma cholesterol levels (C) and atherosclerotic lesions at the aortic root (D-G). (D) A scattered dot plot (left) or representative photomicrographs showing the size of atherosclerotic lesions. Sections were stained with oil-red-O (original magnification 40x, right panel). Each dot represents the mean lesion area of a single mouse, and the horizontal bar indicates the mean value of the group (left panel). (E) Representative photomicrographs showing macrophages and collagens in lesions. Sections of aortic roots were stained with antibodies against Moma-2 to visualize macrophages (brown, 100x) or with Masson’s Trichrome Accustain to visualize collagens (blue, 100x). (F & G) Bar graphs showing the lesion contents of macrophages (F), collagens (G), necrotic core (H) and cap thickness (I). Results were expressed as mean±SEM. Statistically significant difference *p<0.05, **p<0.01, and ***p<0.001 vs vehicle.