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EPC home to bioprosthetic grafts and to balloon-injured carotid arteries.
BM-derived AC133
þ
cells were even able to cover ventricular assist devices
(
Peichev et al., 2000
).
Overall, these studies implicate that regardless of the origin of CEPC, this
pool of CECs may exert an important function as an endogenous repair mech-
anism to maintain the integrity of the endothelial monolayer by replacing
denuded parts of the artery and to cover intracoronary devices. Moreover,
various risk factors for CAD, such as diabetes, hypercholesterolemia, hyper-
tension, and smoking, affect the number and functional activity of EPCs in
healthy volunteers and in patients with CAD (
Hill et al., 2003; Vasa et al.,
2001
). It is also known that circulating levels of these cells are positively cor-
relatedwith endothelial cell colony forming units (EC-CFU) numbers and are
inversely correlated with Framingham risk scores in humans (the Framingham
risk score includes the following parameters: age, cholesterol, systolic blood
pressure, treatment for hypertension, and cigarette smoking and represents
a 10-year risk for developing severe coronary heart disease;
Ghani et al.,
2005; Hur et al., 2007
).
Taking all this into account, EPCs seem to be the kind of cell type, one
would like to augment as much as possible in cardiovascular disease. But
recent studies also have shown that patients with high numbers of EPC
in the PB had a higher risk of in-stent stenosis than patients with lower
EPC counts (
Pelliccia et al., 2010
). Therefore, over the past years, the idea
of EPC participating in atherosclerosis has come more into focus. Already
Campbell et al. (2001)
reported that BM-derived progenitor cells were
found to attach to the endoluminal surface of injured vessel segments,
thereby resulting in the narrowing of the lumen and contributing to the for-
mation of neointima, which also clarifies more of EPC function.
Overall, it can be concluded that EPCs do have a function in acute myo-
cardial ischemia and that they lead to changes in the endothelium. The exact
mechanism of these effects and whether these effects are always beneficial
remain unclear. Further, most of these studies use different ways to identify
EPCs. Therefore, a great heterogeneity of cell types is used in these studies.
To evaluate the exact mechanism of EPC, an exact identification and ter-
minology are crucial.
3.2.2 Cerebral disease
The number of circulating EPChas been associatedwith positive development
after ischemic stroke. The increase in circulating EPC after acute ischemic
stroke was linked with good functional outcome and reduced infarct growth
(
Sobrino et al., 2007
). Further, higher EPC levels were indicative of smaller
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