Blood, Vol. 95 No. 2 (January 15), 2000:
pp. 728-728
CORRESPONDENCE
 |
Letter |
To the editor:
Circulating endothelial cells in acute coronary syndromes
We read with interest Stefanec's1 comments about
our work on circulating endothelial cells (CECs) in acute coronary
syndromes.2 We feel, however, that most of these comments
are inaccurate.
First, Stefanec claims that we found no circulating endothelial cells
in controls. We did in fact find a small number of cells in some
control patients, but these cells were outside the interquartile and
median range that we reported. More specifically, he
indicates that we failed to demonstrate activated or apoptotic
endothelial cells. Regarding cell activation, we clearly stated that a
proportion of isolated cells were positive for tissue factor. If one
accepts that expression of tissue factor is associated with endothelial cell activation,3 then it follows that a proportion of
cells were activated. Furthermore, we also detected apoptotic cells, although these cells represented less than 10% of the total
circulating endothelial cells isolated.
Second, Stefanec points out that our results disagree with those of
Solovey et al.4 We feel this comment inappropriate, since
nowhere in our paper do we contend that our results are directly
comparable with those of Solovey; our two groups used different control
subjects and different methodologies to isolate circulating endothelial cells.
Stefanec goes on to elaborate why, in his view, we have
been unable to identify apoptotic endothelial cells. We agree that the
TUNEL assay is not able to detect early stages of apoptosis. However,
this technique has been validated for detection of apoptosis in major
studies.5,6 Again, the fact that we did find a small proportion of apoptotic endothelial cells disproves Stefanec's statement that our method is not able to identify such cells. We are
also surprised that he contends that acridine orange-staining excludes
apoptotic cells, since many studies have used this reagent to visualize
chromatin condensation and cytoplasm blebbing accompanying apoptosis.7,8 Anyhow, we did not use this method for the purpose of identifying apoptosis in CECs. Finally, many of
the references quoted by Stefanec deal with the anti-apoptotic effect of drugs administered to our patients that would act to reduce the
number and apoptotic state of circulating endothelial
cells.9-14 Although most of these papers refer to in vitro
studies and/or animal models and have used methodologies quite
different from ours, we do not contest this potential effect. Anyway,
even in this hypothesis, our findings of significantly higher levels of non-apoptotic circulating endothelial cells in patients with acute coronary syndromes as compared to controls remain valid, since all
patients and controls were similarly treated. In our opinion, none of
the references quoted by Stefanec is in contradiction with our results
or supports the hypothesis that they could be due to methodological or
therapeutic artifacts.
Françoise Dignat-George
Laboratoire d'Hématologie et d'Immunologie UFR de
pharmacie Marseille, France
Andrew Blann
Haemostasis, Thrombosis and Vascular Biology
Unit University Department of Medicine City Hospital
Birmingham, United Kingdom
José Sampol
Laboratoire d'Hématologie Hôpital de la
Conception Marseille, France
| |
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