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Stem Cells International
Volume 2013, Article ID 859643, 7 pages
Research Article

Coculture with Late, but Not Early, Human Endothelial Progenitor Cells Up Regulates IL-1β Expression in THP-1 Monocytic Cells in a Paracrine Manner

Division of Cardiology, Keenan Research Center, Li Ka Shing Knowledge Institute, St. Michael’s Hospital, University of Toronto, Room 7084 Bond Wing, 30 Bond Street, Toronto, ON, Canada M5B 1W8

Received 9 July 2013; Revised 7 November 2013; Accepted 22 November 2013

Academic Editor: Mark D. Kirk

Copyright © 2013 Qiuwang Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Endothelial progenitor cells (EPCs) have been used in clinical trials to treat ischemic heart disease. Monocyte infiltration plays an important role in inflammation, angiogenesis, and tissue repair during tissue ischemia. It is important to understand the interactions between EPCs and monocytes. In this study, a human EPC/THP-1 monocytic cell coculture system was used to examine EPC effect on IL-1α, IL-1β, and TNF-α expression in THP-1 cells. Late, but not early, EPCs upregulated IL-1β expression at both mRNA and protein levels. In contrast, neither early nor late EPCs affected IL-1α or TNF-α expression. Coculture with human umbilical vein endothelial cells did not alter IL-1β expression. It has been shown that activation of integrin β2 in human neutrophils augments IL-1β synthesis; however integrin β2 was not involved in IL-1β expression in THP-1 cells. Addition of late EPC conditioned medium to THP-1 cell culture led to a modest increase of IL-1β mRNA levels, indicating that late EPCs upregulate IL-1β expression partly through a paracrine pathway. IL-1β, an important inflammation mediator, has been shown to promote EPC function. Our data therefore suggest that late EPCs can exert self-enhancement effects by interacting with monocytes and that EPCs might modulate inflammatory reactions by regulating IL-1β expression in monocytes.