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B-Independent Mechanism1
Department of Cardiothoracic Surgery, National Heart and Lung Institute, Imperial College School of Medicine, Heart Science Centre, Harefield Hospital, Harefield, Middlesex, United Kingdom
ICAM-1 is an Ig-like cell adhesion molecule expressed by several
cell types, including the endothelium. Cross-linking of ICAM-1 on the
surface of different cell types has previously been shown to cause an
increase in cellular activation within the cytoplasm. In this study, we
have compared signaling events following ligation of ICAM-1 by
cross-linking with mAbs with events after activation of HUVEC by TNF.
ICAM-1 cross-linking caused activation of Erk-1 and the AP-1
transcription factor complex, without any increase in NF-
B activity,
in contrast to TNF stimulation. Transcription of VCAM-1 mRNA was
observed by reverse-transcriptase PCR after ICAM-1 cross-linking, with
no associated transcription of E-selectin. This was reflected by the
presence of VCAM-1 protein after immunoprecipitation, without
E-selectin expression, in ICAM-1 cross-linked cells. In contrast, mRNA
and protein for both VCAM-1 and E-selectin were observed in TNF-treated
HUVEC, as expected. Addition of the MEK (MAP/Erk kinase)
inhibitor PD98059 reduced expression of VCAM-1 after ICAM-1
cross-linking, suggesting that the Erk pathway is involved in
ICAM-1-mediated VCAM-1 expression. In conclusion, ICAM-1-induced
expression of VCAM-1 represents a pathway for adhesion molecule
up-regulation that is distinct from the TNF-induced pathway. It may be
similar to the IL-4 pathway or it may represent a novel
pathway.
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