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See Latest ArticlesSirolimus and everolimus induce endothelial cellular senescence via sirtuin 1 down-regulation: Therapeutic implication of cilostazol after drug-eluting stent implantation
JACC - Journal of the American College of Cardiology, 06/11/09
Ota H et al. – Sirolimus and everolimus induce endothelial senescence involving downregulation of mammalian sirtuin 1 (Sirt1). In contrast, development of endothelial senescence by paclitaxel involves a Sirt1-independent pathway. Because sirolimus and everolimus are involved in Sirt1 modulation, cilostazol rescues HUVEC from sirolimus- or everolimus-induced senescence. These results may have therapeutic implications in the clinical sequelae after drug-eluting stent (DES) implantation.
Methods- Study comparing effects of paclitaxel, sirolimus, and everolimus on senescent phenotype in human endothelial cells
- Investigation of possible involvement of Sirt1 downregulation as a mechanism
- Judgement of senescent human umbilical vein endothelial cells (HUVEC) by senescence-associated beta-galactosidase assay (SA-betagal), morphological appearance, and plasminogen activator inhibitor (PAI)-1
- Treatment with paclitaxel, sirolimus, and everolimus significantly caused a senescent phenotype and PAI-1 upregulation, associated with decreased endothelial nitric oxide synthase (eNOS) and Sirt1 expression
- Overexpression of Sirt1 or Sirt1 activation reversed sirolimus- or everolimus-induced senescent phenotype
- Sirt1 overexpression did not suppress paclitaxel-induced senescence, suggesting existence of a different mechanism
- Cilostazol markedly inhibited sirolimus- or everolimus-induced senescent phenotype and PAI-1 upregulation, but had no influence on paclitaxel effects
- Aspirin significantly blunted sirolimus- or everolimus-induced senescence, but neither ticlopidine nor clopidogrel had any effects
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