Advanced glycation end products impair the migration, adhesion and secretion potentials of late endothelial progenitor cells.
Advanced glycation end products impair the migration, adhesion and secretion potentials of late endothelial progenitor cells.
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晚期糖基化终产物损害晚期内皮祖细胞的迁移、粘附和分泌潜力
DOI：
10.1186/1475-2840-11-46
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发表时间：
2012-04-30
影响因子：
9.3
通讯作者：
Cheng M
中科院分区：
文献类型：
--
作者：
Li H;Zhang X;Guan X;Cui X;Wang Y;Chu H;Cheng M
BackgroundEndothelial progenitor cells (EPCs), especially late EPCs, play a critical role in endothelial maintenance and repair, and postnatal vasculogenesis. Advanced glycation end products (AGEs) have been shown to impair EPC functions, such as proliferation, migration and adhesion. However, their role in the regulation of the production of vasoactive substances in late EPCs is less well defined.MethodsPassages of 3~5 EPCs, namely late EPCs, were cultured with different concentrations (0~500 μg/ml) of AGEs, and the apoptosis, adhesion and migration were subsequently determined. The release of vasoactive substances, such as stromal cell-derived factor-1 (SDF-1), nitric oxide (NO), prostaglandin I2(PGI2), plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (tPA), and in addition the activity of superoxide dismutase (SOD), were evaluated by ELISA. At the same time, the gene and protein expressions of CXCR4 were assayed by real-time RT-PCR and western-blot.ResultsAGEs promoted late EPC apoptosis. Moreover, AGEs impaired late EPC migration and adhesion in a concentration-dependent manner. Accordingly, the production of SDF-1 was decreased by AGEs. Although the CXCR4 expressions of late EPCs were up-regulated for AGE concentrations of 50, 100 or 200 μg/ml, a marked decrease was observed for the higher concentration of 500 μg/ml. Furthermore, co-culturing with AGEs decreased the levels of NO, t-PA, PGI2,and the activity of SOD but up-regulated the production of PAI-1.ConclusionOur data provide evidence that AGEs play an important role in impairing late EPC functions, which could contribute to the development of vascular diseases in diabetes.
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DOI：
10.1111/j.1440-1681.2007.04875.x
发表时间：
2008-03-01
影响因子：
2.9
作者：
Jandeleit-Dahm, Karin;Watson, Anna;Soro-Paavonen, Aino
通讯作者：
Soro-Paavonen, Aino
影响因子：
3.7
作者：
Kawabe-Yako R;Ii M;Masuo O;Asahara T;Itakura T
通讯作者：
Itakura T
影响因子：
15.9
作者：
Gallagher, Katherine A.;Liu, Zhao-Jun;Velazquez, Omaida C.
通讯作者：
Velazquez, Omaida C.
影响因子：
7.7
作者：
Loomans, CJM;de Koning, EJP;van Zonneveld, AJ
通讯作者：
van Zonneveld, AJ
影响因子：
7.3
作者：
Liang, Chun;Ren, Yusheng;Wu, Zonggui
通讯作者：
Wu, Zonggui