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01.12.2012 | Original investigation | Ausgabe 1/2012 Open Access

Cardiovascular Diabetology 1/2012

Advanced glycation end products impair the migration, adhesion and secretion potentials of late endothelial progenitor cells

Cardiovascular Diabetology > Ausgabe 1/2012
Hong Li, Xiaoyun Zhang, Xiumei Guan, Xiaodong Cui, Yuliang Wang, Hairong Chu, Min Cheng
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1475-2840-11-46) contains supplementary material, which is available to authorized users.
Hong Li, Xiaoyun Zhang contributed equally to this work.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

HL, XYZ and MC were the principal investigators, involved in designing the study and writing the manuscript. XMG coordinated the study and performed statistical analyses. XDC, YLW and HRC were involved in cell culture, western blot and writing parts of the manuscript. All authors participated in writing the final version of the manuscript.



Endothelial 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.


Passages 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.


AGEs 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.


Our 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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