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B and AP-1
Department of Pathology, The University of Western Ontario, London, Ontario, Canada N6A 5C1
Human endothelial
cells cultured under high glucose (HG) conditions were shown before to
upregulate several basement membrane proteins, including fibronectin
(FN), thus mimicking effects of diabetes. Using human macrovascular
(HUVEC) and microvascular (HMEC) endothelial cell lines, we evaluated
in the present study some of the key molecular signaling events
involved in HG-induced FN overexpression. This expression was shown to
be dependent on endogenous endothelin (ET) receptor-mediated signaling.
We also examined the roles played by protein kinase C (PKC) and the
transcription factors nuclear factor 
B (NF-B) and activating
protein (AP)-1 with respect to such changes. HG, PKC activators, and
ETs (ET-1 and ET-3) that increased FN expression also caused activation of NF-B and AP-1. Inhibitors of both NF-B and AP-1 prevented HG-
and ET-induced FN production. ET receptor blockade also prevented these
HG- and ET-mediated changes. The results of this study indicate that
glucose-induced increased FN production in diabetes may be mediated via ET-dependent NF-B and AP-1 activation.
glucose; endothelial cells; activating protein-1; nuclear
factor-B
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