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Blood, Vol. 94 No. 11 (December 1), 1999:
pp. 3820-3828
Divergent Inducible Expression of P-Selectin and E-Selectin in Mice and
Primates
Longbiao Yao,
Hendra Setiadi,
Lijun Xia,
Zoltan Laszik,
Fletcher
B. Taylor, and
Rodger P. McEver
From the W.K. Warren Medical Research Institute, Departments of
Medicine, Biochemistry and Molecular Biology, and Pathology, University
of Oklahoma Health Sciences Center, and Cardiovascular Biology Research
Program, Oklahoma Medical Research Foundation, Oklahoma City, OK.
We used in vitro and in vivo approaches to examine whether tumor
necrosis factor- (TNF-) and oncostatin M (OSM), cytokines that
bind to distinct classes of receptors, differentially regulate expression of P- and E-selectin in murine and primate endothelial cells. In human umbilical vein endothelial cells, TNF- rapidly increased mRNA for E-selectin but not P-selectin. OSM elicited little
or no change in mRNA for E-selectin, but induced a delayed and
prolonged increase in P-selectin mRNA. TNF- and OSM did not cooperate to further enhance P- or E-selectin mRNA. Intravenous infusion of Escherichia coli, which markedly elevates plasma
lipopolysaccharide and TNF-, increased mRNA for
E-selectin but not P-selectin in baboons. In murine bEnd.3 endothelioma
cells, TNF- and OSM individually and cooperatively increased mRNA
and protein for both P- and E-selectin. Intravenous injection of these
cytokines also individually and cooperatively increased mRNA for P- and
E-selectin in mice. We conclude that the murine P- and E-selectin genes
respond to both TNF- and OSM, whereas the primate P- and E-selectin
genes have much more specialized responses. Such differences should be
considered when extrapolating the functions of P- and E-selectin in
murine models of inflammation to humans.
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