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Updated: Dec 31, 2025
Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
Foam cells promote atherosclerosis progression by releasing CXCL12
Lingxing Li1,2, Zhenlan Du2, Bing Rong1
1The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Qilu Hospital of Shandong University, Jinan, China.
Insights
C-X-C motif chemokine 12 (CXCL12) promotes atherosclerosis (AS) progression by increasing foam cell formation. Inhibiting CXCL12 may offer a new therapeutic strategy for treating AS and cardiovascular diseases.
Area of Science:
- Cardiovascular Research
- Inflammation Biology
- Molecular Medicine
Background:
- Atherosclerosis (AS) is a chronic inflammatory disease underlying cardiovascular diseases (CVDs).
- Foam cell formation is a critical process in AS progression.
- Novel therapeutic targets are needed to manage AS and reduce the burden of CVDs.
Purpose of the Study:
- To investigate the role of C-X-C motif chemokine 12 (CXCL12) in atherosclerosis.
- To explore the potential of targeting CXCL12 for AS treatment.
Main Methods:
- In vitro AS models using THP-1 cells and human aortic vascular smooth muscle cells (HA-VSMCs) treated with oxidized low-density lipoproteins (ox-LDLs).
- Assays included MTT for proliferation, Oil Red O for foam cell formation, and siRNA for CXCL12 suppression.
- An in vivo AS rat model was established and analyzed using histopathology and immunohistochemistry for IBA1 and α-SMA.
Main Results:
- CXCL12 expression was significantly upregulated in in vitro AS models.
- Suppression of CXCL12 reduced AS progression in cell models.
- CXCL12 was found to promote AS in an in vivo rat model.
Conclusions:
- CXCL12 plays a significant role in promoting AS progression.
- Inhibiting CXCL12 may suppress AS development by reducing HA-VSMC proliferation and foam cell transformation.
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.
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