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INHIBITION OF MICROPARTICLE RELEASE TRIGGERS ENDOTHELIAL APOPTOSIS
Abstract number: P-M-437
Abid-Hussein1 M.N., Böing1 A.N., Sturk1 A., Hau1 C.M., Nieuwland1 R.
1Clinical Chemistry, Academic Medical Center, Amsterdam, Netherlands
How-to-cite Abid-Hussein MN, Böing AN, Sturk A, Hau CM, Nieuwland R. INHIBITION OF MICROPARTICLE RELEASE TRIGGERS ENDOTHELIAL APOPTOSIS. J Thromb Haemost 2007; 5 Supplement 2: P-M-437
Abstract
Introduction: Previously, we demonstrated that viable endothelial cell cultures contain caspase 3-containing microparticles. We hypothesize that the release of such microparticles protects endothelial cells from caspase 3 accumulation, detachment and apoptosis.
Methods: Human umbilical vein endothelial cells (HUVEC; n=3) were incubated with (and without) inhibitors of microparticle release (Y-27632 plus calpeptin, both in the absence or presence of additional "external stress", i.e. the apoptotic agent staurosporin (200 nmol/L) or the activating cytokine interleukin (IL)-1alpha (5 ng/mL).
Results: Control cultures contained mainly viable adherent cells and minor fractions of apoptotic detached cells and microparticles in the absence of inhibitors of microparticle release. In the presence of such inhibitors, caspase 3 accumulated in adherent cells (P=0.03) and detachment tended to increase (P=0.07). During incubation with either staurosporin or IL-1alpha in the absence of inhibitors of microparticle release, the adherent cells remained viable, and detachment and EMP release increased only slightly. In the presence of inhibitors, however, dramatic changes occurred in staurosporin-treated cultures. The efficacy of inhibitors to block EMP release, expressed per detached cell, was approximately 80%. Simultaneously, caspase 3 accumulated in adherent cells and >90% of the cells detached within 48 hours (P=0.01). In IL-1alpha-treated cultures no accumulation of caspase 3 was observed in adherent cells, although detachment increased (P=0.02).
Conclusions: Inhibition of microparticle release facilitates accumulation of caspase 3 and promotes detachment, although this depends on the kind of "external stress". Thus, the release of caspase 3-containing microparticles may contribute to endothelial survival.
To cite this abstract use the following format:
Journal of Thrombosis and Haemostasis 2007; Volume 5, Supplement 2: abstract number
Session Details
| Date: |
01/08/2007
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| Time: |
00:00-00:00
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| Session name: |
XXIst ISTH Congress |
| Subject: |
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| Location: |
Oxford, UK |
| Presentation type: |
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