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Low‐dose aspirin promotes endothelial progenitor cell migration and adhesion and prevents senescence
Author(s) -
Hu Zhengli,
Zhang Fumin,
Yang Zhijian,
Zhang Jinying,
Zhang Dingguo,
Yang Naiquan,
Zhang Yuqing,
Cao Kejiang
Publication year - 2008
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2008.03.004
Subject(s) - senescence , enos , progenitor cell , endothelial progenitor cell , mtt assay , fibronectin , apoptosis , dapi , angiogenesis , microbiology and biotechnology , chemistry , flow cytometry , andrology , biology , nitric oxide , stem cell , nitric oxide synthase , cancer research , medicine , biochemistry , endocrinology , extracellular matrix
Circulating endothelial progenitor cells (EPCs) play a key role in restoring endothelial function and enhancing angiogenesis. However, the effects of low‐dose aspirin on circulating EPCs are not well known. We investigated the effects of low‐dose aspirin on EPC migration, adhesion, senescence, proliferation, apoptosis and endothelial nitric oxide synthase (eNOS) expression. EPC migration was detected by a modified Boyden chamber assay. EPC adhesion assay was performed by counting adherent cells on fibronectin‐coated culture dishes. EPC senescence was assessed by both senescence‐associated‐β‐galactosidase staining and DAPI staining. EPC proliferation was analyzed by MTT assay. EPC apoptosis was evaluated by flow cytometric analysis. eNOS protein expression was measured by Western blotting analysis. Aspirin promoted EPC migratory and adhesive capacity at concentrations between 0.1 and 100 μmol/L and prevented senescence at concentrations between 50 and 100 μmol/L. Meanwhile, aspirin in a range of these concentrations did not affect EPC proliferation, apoptosis or eNOS expression. Our findings indicate that low‐dose aspirin promotes migration and adhesion and delays the onset of senescence of EPCs.