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Blood, Vol. 94 No. 6 (September 15), 1999:
pp. 2020-2028
Cultured Endothelial Cells From Human Arteriovenous Malformations
Have Defective Growth Regulation
Marie-Paule Wautier,
Bernadette Boval,
Olivier Chappey,
Odile Enjolras,
Nicolas Wernert,
Jean-Jacques Merland, and
Jean-Luc Wautier
From the Laboratoire de Biologie Vasculaire et Cellulaire,
Unité de Formation et de Recherche Lariboisière-St Louis,
Paris 7, INTS, Paris, France; the Département de
Radiologie Interventionnelle, Hôpital Lariboisière, Paris,
France; and the Institute of Pathology, University of Bonn, Bonn,
Germany.
Vascular malformations are frequent in newborns, and they persist
throughout life, which differentiates them from vascular tumors (eg,
hemangiomas). Arteriovenous malformations are high-flow vascular
malformations. They are considered nonmalignant but can expand and
become a significant clinical risk when extensive. To characterize
endothelial cells from arteriovenous malformations (AMEC), we cultured
cells obtained from surgical specimens and studied their properties.
After selection, the cells that grew out from explants had phenotypic
and antigenic features (platelet endothelial cell adhesion molecule,
von Willebrand factor) of human endothelial cells. Their spontaneous
proliferation rate was higher (1.8 to 6.4 times) than that of human
umbilical vein, arterial, or microvascular endothelial cells. The
proliferation rate of AMEC was not sensitive to the inhibitory activity
of various cytokines (interleukin-1 , tumor necrosis factor- ,
transforming growth factor-, Interferon- ). In basal conditions,
intercellular adhesion molecule (ICAM-1) was detected at a higher level
of expression (6- to 10-fold) on AMEC, but these cells failed to
express E-selectin or the vascular cell adhesion molecule (VCAM-1)
after cytokine stimulation. Expression of c-ets-1 proto-oncogene was
shown by in situ hybridization. The low response to cytokines, the
higher propensity to proliferate, and the ets-1 expression suggest that AMEC have a defective regulation of proliferation that may be due to a
reduced apoptotic process.
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