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J Biol Chem, Vol. 275, Issue 19, 14632-14641, May 12, 2000
From the Departments of Extracellular interactions of plasma clotting
factor VIIa (FVIIa) with tissue factor (TF) on cell surfaces trigger
the intracellular signaling events. At present, it is unclear how these
signals influence phenotype. To elucidate this, we have used cDNA
microarray technology to examine changes in transcriptional program in
human fibroblasts in response to exposure to FVIIa. cDNA
microarrays revealed that FVIIa binding to TF up-regulated the
expression of Cyr61 and CTGF (connective tissue
growth factor), the genes that encode extracellular matrix signaling
proteins Cyr61 and CTGF, respectively. Northern blot analysis confirmed
that FVIIa binding to TF markedly increased the expression of
Cyr61 and CTGF in a time- and
dose-dependent manner. FVIIa catalytic activity is required
for the gene induction. In addition to FVIIa, thrombin also induced the
expression of Cyr61 and CTGF. Hirudin abolished the thrombin-induced expression of these mRNAs but not the
FVIIa-induced expression. FVIIa-induced expression of Cyr61
appears not to involve the currently known protease-activated receptors
(PARs), whereas thrombin-induced expression involves the activation of
PAR1 and possibly an additional PAR. Various intracellular signaling
pathway inhibitors exhibited different inhibitory pattern on FVIIa and thrombin-induced up-regulation of Cyr61. Cyr61 and CTGF
could act as downstream mediators of FVIIa·TF in affecting various
biological processes.
Factor VIIa and Thrombin Induce the Expression of Cyr61 and
Connective Tissue Growth Factor, Extracellular Matrix Signaling
Proteins That Could Act as Possible Downstream Mediators in Factor
VIIa·Tissue Factor-induced Signal Transduction*
§,,
Molecular Biology and
Biochemistry, The University of Texas Health Center at
Tyler, Texas 75708 and the ¶ Tissue Factor/Factor VII Research,
Novo Nordisk A/S Health Care Discovery,
Malov DK-2760, Denmark
*
This work was supported in part by a grant from the American
Heart Association, Texas Affiliate (to U. R. P.) and a grant from
Novo-Nordisk Health Care Discovery (to L. V. M. R.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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