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Blood, Vol. 93 No. 12 (June 15), 1999:
pp. 4293-4299
Induction and Suppression of Endothelial Cell Apoptosis by
Sphingolipids: A Possible In Vitro Model for Cell-Cell Interactions
Between Platelets and Endothelial Cells
Nobuo Hisano,
Yutaka Yatomi,
Kaneo Satoh,
Shigeo Akimoto,
Masako Mitsumata,
Masayuki A. Fujino, and
Yukio Ozaki
From the Department of Laboratory Medicine, First Department of
Pathology and First Department of Internal Medicine, Yamanashi Medical
University, Yamanashi, Japan.
Because sphingosine (Sph) is actively incorporated into platelets
and rapidly converted to sphingosine 1-phosphate (Sph-1-P), which is
then released extracellularly, it is important to study the effects of
Sph and Sph-1-P on endothelial cells from the viewpoint of
platelet-endothelial cell interaction. In this study, we found that
Sph, as well as ceramide, induces apoptosis in human umbilical vein
endothelial cells (HUVECs). In contrast, Sph-1-P acts as a HUVEC
survival factor; this bioactive lipid was shown to protect HUVECs from
apoptosis induced by the withdrawal of growth factors and to stimulate
HUVEC DNA synthesis. In metabolic studies, [3H]Sph,
incorporated into HUVECs, was converted to [3H]Cer and
further to [3H]sphingomyelin in a time-dependent manner,
whereas [3H]Sph-1-P formation from [3H]Sph
was weak and transient. These findings in HUVECs are very different
from those of platelets, which possess a highly active Sph kinase but
lack Sph-1-P lyase. As a result, platelets abundantly store Sph-1-P,
whereas HUVECs contain much less Sph-1-P. Finally, HUVECs, in contrast
to platelets, failed to release Sph-1-P extracellularly, indicating
that HUVECs themselves are not able to supply the survival factor Sph-1-P, but receive it from activated platelets. Our results suggest that platelets may maintain the integrity of endothelial cells
by incorporating Sph and releasing Sph-1-P.
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