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Biochem Biophys Res Commun. 2004 Jul 16;320(1):34-8.

Statin decreases endothelial microparticle release from human coronary artery endothelial cells: implication for the Rho-kinase pathway.

Author information

1
The 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

Abstract

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.

PMID:
15207698
DOI:
10.1016/j.bbrc.2004.05.127
[Indexed for MEDLINE]
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