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Blood, Vol. 95 No. 4 (February 15), 2000:
pp. 1309-1316
Transcriptional activation of urokinase by the Krüppel-like
factor Zf9/COPEB activates latent TGF- 1 in vascular endothelial
cells
Soichi Kojima,
Shinichi Hayashi,
Kentaro Shimokado,
Yasuhiro Suzuki,
Jun Shimada,
Massimo P. Crippa, and
Scott L. Friedman
From the Laboratory of Molecular Cell Sciences, Tsukuba Life Science
Center, The Institute of Physical and Chemical Research (RIKEN),
Koyadai, Tsukuba, Ibaraki 305-0074, Japan; First Department
of Internal Medicine, Nihon University School of Medicine,
Ohyaguchi-kamimachi, Itabashi, Tokyo 173-0032, Japan; National
Cardiovascular Center Research Institute, Osaka 565-0873, Japan;
Laboratory of Molecular Genetics, DIBIT-H. S. Raffaele, Via Olgettina,
Milano 20132, Italy; Division of Liver Diseases, Mount Sinai Medical
Center, New York, New York.
Understanding the regulation of genes controlling fibrinolysis and
matrix homeostasis is essential for elucidating the basis of tissue
repair. A recently described novel Krüppel-like factor, Zf9, is
up-regulated in acute liver injury in activated hepatic stellate cells.
Because Zf9 can be induced widely, its activity was examined in
vascular endothelium, a key cell in vascular injury. Zf9 is induced as
an immediate-early response gene in bovine aortic endothelial cells
(BAECs) following treatment with serum or phorbol ester. Zf9
transcriptionally activates urokinase plasminogen activator (uPA).
Recombinant Zf9-GST binds to wild-type but not mutated `GC-box'
motifs within the human uPA promoter ( 63 to 32), with greatest
affinity to the middle of 3 contiguous GC boxes. Transient transfection
of Zf9 drives transactivation of a full-length uPA promoter- and GC
box-construct, but not a uPA promoter-construct devoid of GC boxes.
Transactivation of uPA by Zf9 is also supported in Drosophila
S2 cells. Most importantly, transiently transfected Zf9 up-regulates
endogenous uPA messenger RNA and activity in BAECs, resulting in
increased bioactive transforming growth factor-beta (TGF- ) via
enhancement of proteolytic activation of the latent molecule.
Furthermore, concomitant expression of Zf9 and uPA proteins was
observed in arterial endothelial cells after balloon injury in rats,
suggesting a potential role of Zf9 in uPA expression not only in vitro
but also in vivo. These findings suggest a role of Zf9 in the injury
response by enhancing uPA synthesis and subsequent activation of latent
TGF-.
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