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Published on: July 10, 2019
Statin decreases endothelial microparticle release from human coronary artery endothelial cells: implication for the
Anthony F Tramontano1, Jeanne O'Leary, Aislinn D Black
1The Department of Pathology, The New York Harbor VA Health Care System, Manhattan Campus, 423 East 23rd Street, New York, NY 10010, USA. antoniotramontano@hotmail.com
Objective:
Elevated plasma levels of endothelial microparticles (EMPs) are associated with the presence of clinical atherosclerosis. Considering the anti-inflammatory properties of HMG-CoA reductase inhibitors on the endothelium, we studied the effect of fluvastatin on the release of EMPs in cultured human coronary artery endothelial cells (HCAEC).
Methods And Results:
EMPs were generated in TNF-alpha-activated HCAECs. The absolute number of EMPs was enumerated using a novel two-color flow cytometric immunostaining technique with TruCount beads as an internal reference. EMPs are defined as EC membrane vesicles (1-2 microm in size) with a characteristic immunophenotype. The addition of fluvastatin to TNF-alpha-activated HCAECs significantly suppressed EMP release. Fluvastatin suppressed TNF-alpha-induced Rho activation. The Rho-kinase inhibitor, Y-27632, reproduced the effect of statin.
Conclusion:
EMP release from TNF-alpha-activated HCAECs is suppressed by fluvastatin. In addition, the Rho/Rho-kinase may play an important role in modulating EMP release.
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