Fibroblast Growth Factor-2 Induces Hepatocyte Growth Factor/Scatter Factor Expression in Osteoblasts1
Hepatocyte growth factor/scatter factor (HGF/SF) is a multifunctional growth factor with a major role in tissue morphogenesis and repair. It stimulates the proliferation of cells of the osteoblast and osteoclast lineages. Mitogenic factors playing a role in fracture repair may act by regulating HGF/...
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Published in | Endocrinology (Philadelphia) Vol. 140; no. 3; pp. 1069 - 1074 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Endocrine Society
01.03.1999
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Online Access | Get full text |
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Summary: | Hepatocyte growth factor/scatter factor (HGF/SF) is a multifunctional
growth factor with a major role in tissue morphogenesis and repair. It
stimulates the proliferation of cells of the osteoblast and osteoclast
lineages. Mitogenic factors playing a role in fracture repair may act
by regulating HGF/SF expression or activity in bone-forming cells. We
investigated the effect of fibroblast growth factor-2 (FGF-2) on the
expression of HGF/SF and its receptor, encoded by c-met, in the
MC3T3-E1 osteoblastic cell line. MC3T3-E1 cells expressed low levels of
HGF/SF messenger RNA (mRNA), which were markedly increased by FGF-2 in
a dose- and time-dependent manner. FGF-2 also induced HGF/SF
polypeptide synthesis. The stimulation of HGF/SF mRNA expression by
FGF-2 was blocked by cycloheximide, a protein synthesis inhibitor, but
not by DNA or prostaglandin synthesis inhibitors. FGF-2 increased the
rate of HGF/SF gene transcription by approximately 2-fold, as
determined by nuclear run-on assays, and did not modify the decay of
HGF/SF mRNA in transcriptionally arrested cells. FGF-2 also caused a
dose- and time-dependent stimulation of c-met mRNA. In conclusion,
FGF-2 induces HGF/SF expression in osteoblasts and may promote HGF/SF
activity by increasing the expression of its receptor. Through these
mechanisms, HGF/SF could mediate FGF actions on bone repair. |
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ISSN: | 0013-7227 1945-7170 |
DOI: | 10.1210/endo.140.3.6553 |