(Circulation. 1999;100:2550.)
© 1999 American Heart Association, Inc.
Correction
In the article by Hubacek et al that appeared in a previous issue of the journal (Circulation. 1999;99:3218–3220), two scientists who contributed significantly to the article were omitted from the author list. This led to some important omissions in the Introduction, Discussion, and Acknowledgments. The correct information follows:
The correct author list is:
Jaroslav A. Hubacek, PhD; Gregor Rothe, MD; Jan Pit’ha,
MD; Zdena 
kodová, MD; Vladimír Stan
k, MD;
Rudolf Poledne, PhD; Gerd Schmitz, MD. Drs Rothe and Schmitz are
affiliated with the Institute of Clinical Chemistry and Laboratory
Medicine, University of Regensburg, Regensburg, Germany.
The second paragraph of the Introduction has been corrected and the following amendment made:
Interestingly, CD14 expression has been shown to be reduced by cholesterol-lowering therapy with fluvastatin, indicating that a lower expression of this receptor may be beneficial for the vascular wall.a In addition, the size of a specific monocyte subpopulation with a lower expression of CD14 and positive for CD16a (CD14dim/CD16+) is positively correlated to several risk factors for arteriosclerosis, including the apoE4/4 genotype.b The latter is also associated with a changed differentiation pattern of monocytes.c The relevance of CD14+ monocytes and their coexpression with other surface receptors that are important in vascular biology has been reviewed recently.d
The third paragraph of the Discussion has been changed:
The described polymorphism in the CD14 gene promoter is located near
the Sp1 recognition sequence, which is necessary for CD14
expression.7 Meisel et al10 recently described
a 30% increased density of CD14 receptors in patients in the acute
phase of MI. Our data in healthy volunteers without acute illness
showed that the C(-260)
T change affects the level of CD14 gene
expression, and thus we suppose that this increased density is
permanent and genetically determined. These combined data and the
results obtained previously by our groupa–d indicate that
an increased expression of CD14 due to genetic, metabolic, or
pharmacological causes may be a risk factor for cardiovascular disease.
Acknowledgments
This work was supported in Prague by grants 4246-2, 3658-3, and 3635-6 from the Internal Grant Agency of the Czech Ministry of Health; grant 306/96/K220 from the Grant Agency of the Czech Republic; and in Regensburg by a grant from the Deutsche Forschungsgemeinschaft and Bayer Pharma Wupperetal (Forschungsgruppe Makrophagen).
Additional References
a. Rothe G, Herr AS, Stöhr J, Abletshauser C, Weidinger G, Schmitz G. A more mature phenotype of blood mononuclear phagocytes is induced by fluvastatin treatment in hypercholesterolemic patients with coronary heart disease. Atherosclerosis. 1999:144:251–261.
b. Rothe G, Gabriel H, Kovacs E, Klucken J, Stöhr J, Kindermann W, Schmitz G. Peripheral blood mononuclear phagocyte subpopulations as cellular markers in hypercholesterolemia. Arterioscler Thromb Vasc Biol. 1996;16:1437–1447.
c. Stöhr J, Schindler G, Rothe G, Schmitz G. Enhanced
upregulation of the Fc
receptor IIIa (CD16a) during in vitro
differentiation of apoE4/4 monocytes. Arterioscler Thromb Vasc
Biol. 1998;18:1424–1432.
d. Schmitz G, Orso E, Rothe G, Klucken J. Scavenging, signalling and adhesion coupling in macrophages: implications for atherogenesis. Curr Opin Lipidol. 1997;8:287–300.
The authors apologize for these errors.
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