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and IFN-
: Critical Role of STAT-1
1
Department of Cell Biology, University of Alabama, Birmingham, AL 35294
Matrix metalloproteinases (MMPs) are a family of zinc-dependent
endopeptidases that play crucial roles in proteolytic degradation of
the extracellular matrix. Aberrant expression of the 92-kDa type IV
collagenase (MMP-9) is implicated in the invasion and angiogenesis
process of malignant tumors and in inflammatory diseases of the CNS. We
investigated the effects of IFN-
and IFN-
, cytokines used for
treating some cancers and multiple sclerosis, on MMP-9 expression in
human astroglioma and fibrosarcoma cell lines and primary astrocytes.
Our results demonstrate that IFN- and IFN- significantly inhibit
MMP-9 enzymatic activity and protein expression that is induced by PMA
and the cytokine TNF-
. The inhibitory effects of IFN- and IFN-
on MMP-9 expression correlate with decreased steady state MMP-9 mRNA
levels and suppression of MMP-9 promoter activity. IFN-- and
IFN--mediated inhibition of MMP-9 gene expression is dependent on
the transcription factor STAT-1, since IFN- and IFN- fail to
suppress MMP-9 expression in STAT-1-deficient primary astrocytes and
human fibrosarcoma cells. Reconstitution of human STAT-1
successfully restores the inhibitory effects of IFN- and IFN- on
MMP-9 gene expression. Thus, these data demonstrate the critical role
of STAT-1 in IFN- and IFN- suppression of MMP-9 gene
expression.
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