Endothelial Progenitor Cells—Potential New Avenues to Improve Neoangiogenesis and Reendothelialization - International Review of Cell and Molecular Biology - page 65

Moreover, EPCmay serve as a biological marker for endothelial dysfunction
in patients with chronic pulmonary diseases.
In summary ( Section 3 ), EPC counts differ strongly interindividually and
can be changed by physical exercise. During physical exercise, EPC counts
are higher than at rest and EPC counts are higher as well in trained subjects
compared with untrained subjects. High levels of EPC have been described
as positive markers for the outcome of cerebral disease or MI. The role of
EPC during MI has been described extensively and is indisputable. The pos-
itive effect of EPC on the regenerative process of ischemic tissue is also
widely accepted.
EPCs are also mobilized after different sorts of trauma, including skin-,
bone- and vascular trauma. Surgical interventions also mobilize EPC to an
extent, depending on the extensiveness of the intervention. The role of EPC
in tumor biology is disputable. Whereas some studies have described the
involvement of EPC in the neoangiogenesis of tumor tissue, this was not
always reproducible. An involvement of CAC or ECFC has been advocated
several times but still is not proven completely.
A small number of studies have focused on the involvement of EPC in
pulmonary disease. The findings suggest that EPCs are involved in chronic
pulmonary disease. Overall, it can be stated that during trauma or MI EPC
are strongly mobilized from BM and home to ischemic areas. EPCs seem to
home in these situations to injured vessel walls and have been found to
incorporate in vessel walls. Elevation of EPC count in the PB occurs in acute
diseases involving vascular repair, such as AMI, stroke, vascular damages,
whereas a reduction in EPC migratory function and CFU count is a more
typical feature of chronic pathologies, with an inverse relationship to the
progression or stage of the disease.
4. EPC - DRUG INTERACTIONS
4.1. HMG-CoA inhibitors
Multiple studies have proved the use of a 3-hydroxy-3-methylglutaryl-
coenzyme A (HMG-CoA) inhibitor as simvastatine leads to an increase in
CEPC ( Llevadot et al., 2001; Walter et al., 2002 ). This increase is based
on the recruitment of EPC from BM but it is not cytokine-mediated
( Llevadot et al., 2001; Spadaccio et al., 2010 ). The effect seems to be based
on an activation of the Akt protein kinase pathway by HMG-CoA inhibitors
as simvastatine. In an animal study by Llevadot et al. (2001) , an activation of