Aim:  Atherosclerosis involves the infiltration of inflammatory cells monocytes; however, the fate of infiltrated monocytes to become deleterious M1 or beneficial M2 macrophages at acute stage of the atherosclerosis (ATH) is not fully understood. Moreover, whether bone morphogenetic protein (BMP)-7 has any influence on infiltrated monocytes in acute atherosclerosis needs investigation. 
Methods:  ApoE KO mice (10±2 weeks old) using the partial left carotid artery ligation (PLCA) model which induces low blood flow stress. Blood velocity function was examined with echocardiography, and carotid arteries were collected for histological, biochemical and further analysis in acute stages of atherosclerosis at D5.
Results: A decreased trend in the plaque formation in PLCA+BMP-7 group compared with PLCA was observed. A significant increase (p<0.05) in infiltrated monocytes, and M1 macrophages whereas a decrease in M2 macrophages and arginase 1 was observed in PLCA group compared to control. Furthermore, BMP-7 treatment decreased inflammatory monocytes, M1 macrophages but an increase in anti-inflammatory M2 macrophages, and arginase 1. Moreover, our data shows significant (p<0.05) increase in cell signaling proteins (pP38 and pJNK pathway) and a decrease in pro-survival proteins (PI3K and pERK) in PLCA group and these protein expression was reversed with BMP-7 treatment. A significant (p<0.05) decrease in blood velocity in the PLCA group was improved with BMP-7 treatment. 
Conclusion: Our data in acute stages of atherosclerosis suggest a significant increase in infiltrated monocytes which BMP-7 differentiates into M2 macrophages, and this process is mediated through the PI3K and MAP Kinase pathways.

03 - BMP-7 TREATMENT DIFFERENTIATES INFILTRATED MONOCYTE INTO M2 MACROPHAGES MEDIATED THROUGH PI3K AND MAP KINASE PATHWAYS IN APOE KO MICE