Autocrine/paracrine induction of tissue inhibitor of metalloproteinase-1 in chinese hamster ovary cells by oncostatin M

Chinese hamster ovary (CHO) cells expressing recombinant human oncostatin M (rOM) were found to secrete high levels of a 28-kDa protein. Sequence analysis of the protein suggested that it was hamster tissue inhibitor of metalloproteinase-1 (TIMP-1). In this study, we show that induction of TIMP-1 mR...

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Bibliographic Details
Published in:Matrix biology 1995-10, Vol.14 (8), p.677-680
Main Authors: Malik, Najma, Evans, Beth E., Greenfield, Brad W., Shapiro, Robert A., Hanson, Marcia, Shoyab, Mohammed
Format: Article
Language:English
Subjects:
Animals
Chinese hamster ovary cells
CHO Cells
Cricetinae
Glycoproteins - genetics
Glycoproteins - metabolism
Metalloendopeptidases - antagonists & inhibitors
metallproteinase
Oncostatin M
Peptides - pharmacology
Protease Inhibitors - metabolism
Recombinant Proteins - pharmacology
RNA, Messenger - biosynthesis
Tissue Inhibitor of Metalloproteinases
Transfection
Up-Regulation
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Summary:Chinese hamster ovary (CHO) cells expressing recombinant human oncostatin M (rOM) were found to secrete high levels of a 28-kDa protein. Sequence analysis of the protein suggested that it was hamster tissue inhibitor of metalloproteinase-1 (TIMP-1). In this study, we show that induction of TIMP-1 mRNA and protein by CHO cells is due to rOM action in an autocrine/paracrine mode. TIMP-1 expression in rOM-producing CHO cells increased concomitantly with methotrexate-induced rOM amplification. TIMP-1 upregulation was not caused by either transfection of nonspecific DNA nor was it a direct effect of treatment of the cells with methotrexate. These results suggest that oncostatin M is a potent inducer of TIMP-1 and that its receptor-mediated expression is conserved across species.
ISSN:0945-053X
1569-1802
DOI:10.1016/S0945-053X(05)80031-9