ప్రోటీమిక్స్ & బయోఇన్ఫర్మేటిక్స్ జర్నల్
అందరికి ప్రవేశం
ISSN: 0974-276X
ISSN: 0974-276X
Esther Serrano-Pertierra, Lorena Benavente, Miguel Angel Blanco-Gelaz, Jose Luis Fernandez-Martin, Carlos H Lahoz, Sergio Calleja, Carlos Lopez-Larrea and Eva Cernuda-Morollon
Background: Microparticles are present in low concentrations in normal plasma, but increase in several diseases including atherosclerosis, mainly through membrane activation processes or during apoptosis. The number of circulating microparticles has been proposed as a marker of subclinical atherosclerosis, but their potential role in its progression has not been fully characterized.
Methods: Microparticles released by vascular smooth muscle cells treated with lysophosphatidylcholine were isolated and their composition characterized by proteomic techniques. Some hits were confirmed by western blot in this and other cell lines involved in atherosclerosis. Platelet poor plasma was obtained from patients suffering from carotid stenosis (>70%) by venipuncture and subsequential centrifugation. Platelet poor plasma was analyzed by flow cytometry and the microparticle fraction was analyzed by SDS-PAGE.
Results: Among the proteins identified as components of vascular smooth muscle cells-derived microparticles, caveolin-1 was confirmed by western blot. Caveolin-1 is detected in endothelial cell and fibroblast-derived microparticles but not in those released by other cell types involved in atherosclerosis progression. Caveolin-1 was detected in the microparticle fraction in 73.33% of patients compared to 15.38% of controls. The presence of Caveolin-1 did not correlate with the counts of circulating endothelial-derived microparticles.
Conclusions: Pro-atherogenic stimuli induce the release of microparticles containing Caveolin-1 by vascular smooth muscle cells and endothelial cells. Caveolin-1 is detected in microparticles isolated from plasma obtained from patients suffering from atherosclerosis. Due to its role in the regulation of smooth muscle cell proliferation we hypothesize that the release of microparticles in response to pro-atherogenic stimuli may be involved in the progression of the disease through the regulation of caveolin-1 levels in vascular smooth muscle cells.