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Erschienen in: Clinical Research in Cardiology 2/2011

01.02.2011 | Original Paper

Rosuvastatin induces apoptosis in CD4+CD28null T cells in patients with acute coronary syndromes

verfasst von: Andreas Link, Simina Selejan, Lisa Hewera, Felix Walter, Georg Nickenig, Michael Böhm

Erschienen in: Clinical Research in Cardiology | Ausgabe 2/2011

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Abstract

Aims

CD4+CD28null cells represent an aggressive and long-living T cell subpopulation, capable of infiltrating atheromatous plaque, leading to destabilisation and resulting in acute coronary syndromes (ACS). The aim of this study was to evaluate whether statins decrease the number of circulating CD4+CD28null T cells by apoptosis in patients with ACS.

Methods and results

Patients with troponin-positive ACS (n = 35) without cholesterol lowering drugs were randomised to placebo (n = 17) or rosuvastatin 20 mg (n = 18) once daily for 6 weeks. CD4+CD28null T cell abundance (>1%) was distributed equally among the two groups at entry (n = 10 per group). Within 72 h rosuvastatin treatment significantly reduced mean CD4+CD28null T cell numbers (37 × 106/L vs. placebo 122 × 106/L, n = 20, P = 0.041), IFN-γ production (62.6 vs. 101.5%, P = 0.049) and increased apoptosis of these T cells (63.4 vs. 12.3%, P < 0.001). The intrinsic mitochondria-dependent pathway measured by the anti-apoptotic protein expression of B cell lymphoma 2 (BCL-2) was significantly down-regulated (mean fluorescence intensity 16.08 vs. placebo 43.34, P < 0.001).

Conclusions

The down-regulation of anti-apoptotic BCL-2 expression by statins induces apoptosis in CD4+CD28null T cells. Targeting CD4+CD28null T cells in ACS statins could provide one further therapeutic strategy to prevent acute life-threatening coronary events.
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Metadaten
Titel
Rosuvastatin induces apoptosis in CD4+CD28null T cells in patients with acute coronary syndromes
verfasst von
Andreas Link
Simina Selejan
Lisa Hewera
Felix Walter
Georg Nickenig
Michael Böhm
Publikationsdatum
01.02.2011
Verlag
Springer-Verlag
Erschienen in
Clinical Research in Cardiology / Ausgabe 2/2011
Print ISSN: 1861-0684
Elektronische ISSN: 1861-0692
DOI
https://doi.org/10.1007/s00392-010-0225-8

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