Open Access Open Badges Research article

Genetic module and miRNome trait analyses reflect the distinct biological features of endothelial progenitor cells from different anatomic locations

Cheng-Chung Cheng1, Hung-Hao Lo2, Tse-Shun Huang2, Yi-Chieh Cheng2, Shi-Ting Chang3, Shing-Jyh Chang4 and Hsei-Wei Wang2356*

Author Affiliations

1 Division of Cardiology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan

2 Institute of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan

3 Institute of Biomedical Informatics, National Yang-Ming University, No. 155, Sec 2, Li-Nong Street, Taipei, Taiwan

4 Department of Obstetrics and Gynecology, Hsinchu Mackay Memorial Hospital, Hsinchu, Taiwan

5 Department of Education and Medical Research, Taipei City Hospital, Taipei, Taiwan

6 National Yang-Ming University VGH Genome Research Center, National Yang-Ming University, Taipei, Taiwan

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BMC Genomics 2012, 13:447  doi:10.1186/1471-2164-13-447

Published: 3 September 2012



Endothelial progenitor cells (EPCs) play a fundamental role in post-natal vascular repair, yet EPCs from different anatomic locations possess unique biological properties. The underlying mechanisms are unclear.


EPCs from CB expressed abundant genes involved in cell cycle, hypoxia signalling and blood vessel development, correlating with the phenotypes that CB-EPCs proliferated more rapidly, migrated faster, and formed tubule structure more efficiently. smRNA-seq further deciphered miRNome patterns in EPCs isolated from CB or PB: 54 miRNAs were enriched in CB-EPCs, while another 50 in PB-EPCs. Specifically, CB-EPCs expressed more angiogenic miRNAs such as miR-31, while PB-EPCs possessed more tumor suppressive miRNAs including miR-10a. Knocking down miR-31 levels in CB-EPCs suppressed cell migration and microtubule formation, while overexpressing miR-31 in PB-EPCs helped to recapitulate some of CB-EPC functions.


Our results show the foundation for a more detailed understanding of EPCs from different anatomic sources. Stimulating the expression of angiogenic microRNAs or genes in EPCs of low activity (such as those from patients with cardiovascular diseases) might allow the development of novel therapeutic strategies.