Silencing of the F11R gene reveals a role for F11R/JAM-A in the migration of inflamed vascular smooth muscle cells and in atherosclerosis

Atherosclerosis
Bani M AzariA Babinska

Abstract

Our previous studies have determined that the F11 receptor (F11R; aka JAM-A) exerts a critical force in the adhesion of human platelets to inflamed endothelial cells (ECs), and thus can play a significant role in the initiation of atherosclerotic plaque formation. In the present study, we focus on a subsequent event in plaque development--the migration of smooth muscle cells (SMCs) from the media to the intima of inflamed vessels. Here we report our investigation of the expression of F11R in atherosclerotic arteries of coronary artery disease (CAD) patients, and of the role of F11R in the migration of SMCs involved in atherogenesis. Histological staining and specific-antibody immunofluorescence of excised, human atherosclerotic coronary arteries revealed the expression of F11R in the SMCs of the intima. RT-PCR and SDS-PAGE followed by immunoblotting procedures demonstrated that F11R mRNA and the F11R protein levels were enhanced by the stimulation of cultured human aortic SMCs with a combined treatment of proinflammatory cytokines (TNFalpha+INFgamma+IL-beta1). Neither the F11R message nor protein was expressed in non-stimulated SMCs. The functional role of F11R in SMCs' migration was studied in cytokine-stimulated SMCs by inter...Continue Reading

References

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Jun 3, 2006·Arteriosclerosis, Thrombosis, and Vascular Biology·Marianna PapaspyridonosLisa Patel
May 8, 2007·Journal of Investigative Medicine : the Official Publication of the American Federation for Clinical Research·Moro O SalifuAnna Babinska
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Citations

Aug 19, 2011·International Journal of Biological Sciences·Pengke YanZhengrong Mei
Aug 1, 2015·Molecular Biology of the Cell·David W ScottKeith Burridge
Aug 1, 2015·International Journal of Rheumatic Diseases·Tzu-Jung FangJeng-Hsien Yen
Sep 18, 2021·Molecular and Cellular Biochemistry·Kamila Czubak-ProwizorMaria Swiatkowska

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