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Divergent JAM-C Expression Accelerates Monocyte-Derived Cell Exit from Atherosclerotic Plaques
Paul F Bradfield1, Arjun Menon2, Marijana Miljkovic-Licina1
1Department of Pathology and Immunology, CMU, University of Geneva, 1211, rue Michel Servet 1, Geneva 4, Switzerland.
Plos One
|July 22, 2016
Summary
Blocking Junctional Adhesion Molecule C (JAM-C) facilitates reverse migration of monocytes from atherosclerotic plaques. This JAM-C interference offers a novel therapeutic strategy to reduce plaque size and chronic inflammation.
Area of Science:
- Cardiovascular Biology
- Immunology
- Cell Biology
Background:
- Atherosclerosis is a chronic inflammatory disease characterized by monocyte accumulation in plaques.
- Current treatments face challenges in preventing monocyte and macrophage buildup within atherosclerotic lesions.
- Junctional Adhesion Molecule C (JAM-C) on vascular endothelium promotes unidirectional monocyte migration into plaques, exacerbating inflammation.
Purpose of the Study:
- To investigate the role of JAM-C in monocyte reverse transendothelial migration and its potential for plaque regression.
- To determine if interfering with JAM-C can facilitate the exit of monocyte-derived cells from inflamed atherosclerotic plaques.
Main Methods:
- Utilized a mouse model of atherosclerosis (ApoE-/-) and human endothelial cells in vitro.
- Manipulated JAM-C expression (overexpression and gene silencing) in endothelial cells under inflammatory flow conditions.
- Administered JAM-C blockade in recipient mice transplanted with atherosclerotic aortic arches.
Main Results:
- Overexpression or silencing of JAM-C in human endothelium increased monocyte reverse transendothelial migration.
- JAM-C blockade in vivo led to enhanced emigration of monocyte-derived cells from atherosclerotic plaques.
- Blocking JAM-C significantly reduced the size of atherosclerotic plaques in mice.
Conclusions:
- JAM-C acts as a unidirectional barrier for leukocyte migration at homeostatic levels.
- Interfering with JAM-C promotes the emigration of atherogenic monocytes/macrophages from plaques.
- JAM-C blockade presents a promising therapeutic avenue for atherosclerosis and other chronic inflammatory diseases.
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