The « semicarbazide sensitive amine oxidase » (SSAO) transforms primary amines into aldehydes, ammonia and hydrogen peroxide and is widely expressed by vascular smooth muscle cells (SMC) from the arterial wall. SSAO expression is increased during VSMC differentiation like in others cell types (adipocytes, chondrocytes). Disregulation of VSMC phenotype participates to the development of atherosclerosis lesion. To evaluate if the absence of SSAO could participate to the development of atherosclerosis, the laboratory established a double ApoE/SSAO knock out mice model (ApoE-/-SSAO-/-).

25 week-old ApoE-/-SSAO-/- mice presented a significant 50 % increase in plaque surface associated with an 80% decrease in a-actin expression in the media of aortic sinus from ApoE-/-SSAO-/- mice compared to ApoE-/- mice. We noticed a small T-cell infiltration in the media from ApoE-/-SSAO-/- mice whereas no T-cell infiltration was observed in the media from ApoE-/- mice. No difference was detected in monocytes/ macrophages infiltration in the plaque in aortic sinus from APOE-/-SSAO-/- mice and ApoE-/-. ApoE-/-SSAO-/- and ApoE-/- mice were transferred with labelled CD45.1 peripheral bone marrow cells from wild type mice. 5 day after PBMC injection, the number of labeled CD45.1 cells was increased in aorta, decreased in blood and unchanged in spleen from ApoE-/-SSAO-/- mice compared to ApoE-/- mice.

In conclusion, the absence of the SSAO increases the atherosclerosis in ApoE-/- mice. This result could be explained by a switch of VSMC to an inflammatory phenotype.