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NDT Advance Access originally published online on February 15, 2008
Nephrology Dialysis Transplantation 2008 23(7):2129-2132; doi:10.1093/ndt/gfn029
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Circulating microparticles in renal diseases

Laurent Daniel1,2, Laetitia Dou3, Yvon Berland4, Philippe Lesavre5, Lise Mecarelli-Halbwachs5 and Francoise Dignat-George3,6

1 Department of Pathology, CHU Timone-Adultes 2 UMR 911 INSERM, Université de la Méditerranée 3 UMR-S 608 INSERM, Université de la Méditerranée 4 Department of Nephrology, CHU Conception, Marseille 5 Department of Nephrology, CHU Necker and INSERM 507, Paris 6 Department of Haematology, CHU Conception, Marseille, France

Correspondence and offprint requests to: Laurent Daniel, Hopital Timone - Anatomo-Pathologie 264 rue st-pierre Marseille 13005, France. Tel: +334-9138-5531; Fax: +334-9138-4411; E-mail: laurent.daniel@ap-hm.fr

Keywords: atherosclerosis; microparticles; renal failure; vasculitis

The first 10% of the full text of this article appears below.



   Introduction
 
Cellular microparticles (MP) are submicrometric fragments resulting from the remodelling of the plasma membrane in response to numerous conditions, including activation and apoptosis [1]. The general consensus is that MP are small (<1 µm), expose the anionic phospholipid phosphatidylserine (PhtdSer) and express membrane antigens that reflect their cellular origin. These characteristics discriminate MP from exosomes, which are smaller (<0.1 µm), originate from intracellular multivesicular bodies and differ in antigenic composition [2].

MP formation, composition and functions
All cell types shed MP according to an active process controlling plasma membrane remodelling and antigenic turnover. Among the mechanisms proposed, disruption of the natural asymmetric distribution of membrane phospholipids is thought to be an important step explaining the translocation of PhtdSer to the exoplasmic leaflet before membrane blebbing and MP shedding. Although calcium entry, activation of calpains and scramblase activity have been reported to be . . . [Full Text of this Article]

MP measurement and variations in atherosclerotic vascular diseases
MP in renal diseases
MP are both causes and consequences of vascular dysfunction (Figure 1)


   Conclusion
 

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