BACKGROUND: Atherosclerosis (AS) is a chronic inflammatory disease that 
contributes to multiple cardiovascular diseases (CVDs), and foam cell formation 
plays important roles in the progression of AS. There is an urgent need to 
identify new molecular targets for treating AS, and thereby improve the quality 
of life and reduce the financial burden of individuals with CVD.
METHODS: An in vitro model of AS was generated by treating THP-1 cells and human 
aortic vascular smooth muscle cells (HA-VSMCs) with oxidized low-density 
lipoproteins (ox-LDLs). HA-VSMC proliferation and foam cell formation were 
detected by the MTT assay and Oil Red O staining. C-X-C motif chemokine 12 
(CXCL12) expression was suppressed by siRNA. An AS rat model was established by 
feeding rats a high-fat diet and vitamin D2 for 3 weeks. Histopathology 
examinations were conducted by Hematoxylin and Eosin (H&E) staining and the 
levels ionized calcium-binding adapter molecule 1 (IBA1) and α smooth muscle 
actin (α-SMA) expression were determined by ELISA assays and 
immunohistochemistry.
RESULTS: An in vitro model of AS was established with THP-1 cells. CXCL12 
expression in the model THP-1 cells was significantly increased when compared 
with its expression in control cells. Suppression of CXCL12 expression reduced 
the progression of AS in the cell model. Moreover, CXCL12 promoted AS in the in 
vivo rat model.
CONCLUSION: Our results suggest that CXCL12 plays an important role in promoting 
the progression of AS. Furthermore, inhibition of CXCL12 might suppress the 
development of AS by inhibiting HA-VSMC proliferation and their transformation 
to foam cells.