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et al., 2009 ). All of these studies reported that the extent of the burn, mean-
ing the percentage of burned body surface, correlated strongly to the mobi-
lization of EPC. Furthermore, this increase was five to ninefold compared
with the levels of controls. Foresta et al. found that about half of the initially
recruited EPC showed signs of apoptosis, which leads to the conclusion that
this massive mobilization is due to a functional impairment of EPC due to
trauma. Further correlations between EPC count and SDF-1 ( Foresta et al.,
2011; Fox et al., 2008 ) as well as VEGF ( Groger et al., 2010; Piatkowski
et al., 2009 ) were seen and discussed as mobilizing factors and/or cytokines
secreted by EPC. An involvement of EPC during the formation of granu-
lation tissue was also discussed ( Foresta et al., 2011 ).
Further, the amount of EPCmobilized was seen to be a predicitive factor
for the outcome of patients with burn injury ( Piatkowski et al., 2009 ). Since
burn injury, which is known to be one of the most severe trauma to the skin,
has an influence on the levels of circulating EPC, it seems to be clear that skin
injury itself is a stimulus for the mobilization of EPC. Morris et al. were able
to prove this concept by wounding 8- to 10-week-old female FVB/NJ
mice. The extent of mobilized EPC was measured by flow cytometry
and by immunohistochemistry ( Morris et al., 2010 ). The skin wounding
led to a liberation of EPC from BM through a mechanism involving
SDF-1 without elevating significantly the plasma levels of SDF-1. This
involvement of EPC in cutaneous wounding is consistent with the results
of the study described by Suh et al. in that transplanted CAC were found
in granulation tissue of mice after wounding ( Suh et al., 2005 ). This supports
the theory that EPC are involved in the mechanism of dermal regeneration.
Overall, the association of EPC in trauma situations has not been studied
sufficiently. Interestingly, one study focused on the serum of polytrauma-
patients and its effect on EPC in vitro ( Henrich et al., 2004 ). The effects
on EPC were attributed mostly to TGF-
b
and VEGF, but further studies
on this topic are missing.
3.2.4 Surgical interventions
As traumatic events are able to induce an increase in circulating EPC, surgical
procedures should be able to do the same. A small number of studies have
looked into this. Condon et al. studied this phenomenon in 2004 in mice
undergoing laparotomy. The surgical intervention group showed increases
in BM and splenic EPC levels at 24 h and in circulating EPC levels at 48 h
compared with control-mice ( Condon et al., 2004 ). Compliant with this data,
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