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CEPC, CAC, and CFU in patients with RA. CEPCs, CACs, and CFUs were
significantly decreased in patients with RA compared with healthy controls
(
Grisar et al., 2005
). Additionally, CEPC counts were correlated inversely
with disease activity. Also in patients with low disease activity, no significant
changes in CEPC, CAC, and CFU counts were seen (
Grisar et al., 2005
). But
the changes in inflammatory diseases are not just restricted to cell count
changes. As Avouac et al. have shown, EPCs undergo also genetic changes
in patients with SSc. A differential expression of TNF-
-induced protein 3
and prostaglandin-endoperoxide synthase 2 were just two of the most evident
changes in the gene profile of ECFC (
Avouac et al., 2011
).
Further, the differential expression of a large group of genes involved in
cell-cell interaction in ECFC from SSc patients suggested a proadhesive pro-
file. This proadhesive profile seems to be one further adjunct that leads to a
decrease in CEPC in inflammatory diseases with a homing of EPC to synovia
and thus a decreased vasculogenesis (
Silverman et al., 2007; Szekanecz et al.,
2010
). The depletion of circulating EPCs and defective vasculogenesis may
therefore be linked to atherosclerosis in RA (
Akhavani et al., 2007; Pakozdi
et al., 2009
).
a
3.2.8 Pulmonary disease
Little is known over the involvement of EPC in pulmonary diseases. One of
the hypotheses that leads to the assumption of EPC involvement in pulmo-
nary diseases is based on the theory of hypoxia-induced mobilization of
CEPC after AMI (
Assmus et al., 2002; Kawamoto et al., 2001; Schuh
et al., 2008
). A second indicator for the involvement of EPC are two animal
studies that linked a decreased VEGF expression in the lung to chronic
obstructive pulmonary disease (COPD;
Kasahara et al., 2001; Tuder
et al., 2003
) and therefore concluded that EPC would also be affected by
this since endothelial dysfunction represents a key part in pulmonary diseases
(
Huertas and Palange, 2011
). As in other diseases, cell counts could be linked
to the severity of the disease in COPD patients (
Palange et al., 2006
). Like-
wise, ECFC and CFU numbers are decreased in COPD patients compared
with healthy controls, and the migratory capacity of ECFCwas also reduced.
Similar findings were described in a study conducted on children with
obstructive sleep apnea (OSA) that investigated EPCs and endothelial dys-
function. In this study, EPC levels were significantly lower in the OSA
group with endothelial dysfunction as compared with control subjects.
These findings suggest that EPCs are involved in chronic pulmonary diseases
and that the disease affects not only their amount but also their function.
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