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CCL11 (Eotaxin) induces CCR3-dependent smooth muscle cell migration
Ravindra B Kodali1, William J H Kim, Irfan I Galaria
1Zena and Michael A. Wiener Cardiovascular Institute and Department of Medicine, The Mount Sinai School of Medicine, New York, NY, USA.
Summary
Vascular smooth muscle cells (SMCs) express the receptor CCR3, which mediates their migration in response to CCL11 (eotaxin). This suggests CCL11 may drive SMC migration in vascular diseases like atherosclerosis.
Area of Science:
- Vascular Biology
- Immunology
- Cell Signaling
Background:
- CCL11 (eotaxin) is a chemokine that attracts eosinophils and is found in atherosclerotic plaques.
- CCR3 is the primary receptor for CCL11 and is expressed on various leukocytes and some nonleukocytic cells.
Purpose of the Study:
- To investigate whether vascular smooth muscle cells (SMCs) express functional CCR3.
- To determine the role of CCL11 and CCR3 in SMC migration.
Main Methods:
- Reverse transcription-polymerase chain reaction (RT-PCR) to detect CCR3 mRNA in mouse aortic SMCs.
- Western blot analysis and flow cytometry to confirm CCR3 protein expression.
- Modified Boyden chamber and scrape-wound assays to assess SMC chemotaxis and migration.
- In vivo femoral artery injury model to evaluate CCR3 and CCL11 expression in injured arteries.
Main Results:
- CCR3 mRNA and protein were detected in mouse aortic SMCs.
- CCL11 induced concentration-dependent SMC migration, which was inhibited by anti-CCR3 antibody.
- CCL11 did not affect SMC proliferation.
- CCR3 and CCL11 expression increased in SMCs after arterial injury, coinciding with a migratory phenotype.
Conclusions:
- SMCs express functional CCR3, mediating CCL11-induced migration.
- CCL11 is a potent chemotactic factor for SMCs.
- CCL11 may play a significant role in regulating SMC migration in atherosclerosis and injured arteries.