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(Received for publication, January 17, 1996, and in revised form, April 5, 1996)
From the Departments of Matrix metalloproteinases participate in normal
physiologic processes; however, their overproduction has been
associated with connective tissue destruction in a variety of
pathological states. Migrating basal keratinocytes transiently express
collagenase-1 during normal cutaneous reepithelialization. However, the
overexpression of both collagenase-1 and stromelysin-1 has been
associated with the pathogenesis of chronic nonhealing ulcers. Aberrant
expression of metalloproteinases in inflammation is mediated, at least
in part, by soluble factors. Since hepatocyte growth factor/scatter
factor (HGF/SF) has been reported to promote keratinocyte migration and
proliferation, key events in wound repair, and since HGF/SF is produced
by dermal fibroblasts and its c-Met receptor is expressed by basal
keratinocytes in wounded skin, we have studied the effects of HGF/SF
upon keratinocyte metalloproteinase expression. We have found that
HGF/SF can stimulate keratinocyte collagenase-1 and stromelysin-1
production in a dose-dependent and
matrix-dependent manner. Expression of 92-kDa gelatinase
was not affected by HGF/SF. We determined that HGF/SF regulation of
collagenase-1 expression is transcriptionally mediated and requires
tyrosine kinase and protein kinase C activaties. HGF/NK1, a naturally
occurring, truncated form of HGF/SF, also stimulates collagenase-1
production, but much less efficiently than does the parent molecule.
However, HGF/NK2, another HGF/SF splice variant, as well as heparin,
potently inhibit HGF/SF-induced collagenase-1 synthesis. These results
indicate that HGF/SF and its naturally occurring splice variants have
diverse biological effects on keratinocytes and suggest an additional
mechanism whereby HGF/SF may regulate keratinocyte function during
wound repair.
Volume 271, Number 40,
Issue of October 4, 1996
pp. 24576-24582
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
,
,
and
Medicine (Dermatology) and
Cell Biology and Physiology, Washington University School of
Medicine, St. Louis, Missouri 63110 and the ¶ Laboratory of
Cellular and Molecular Biology, National Cancer Institute,
Bethesda, Maryland 20892
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