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Expression and induction of collagenases (MMP‐8 and ‐13) in plasma cells associated with bone‐destructive lesions
Author(s) -
Wahlgren Jaana,
Maisi Päivi,
Sorsa Timo,
Sutinen Meeri,
Tervahartiala Taina,
Pirilä Emma,
Teronen Olli,
Hietanen Jarkko,
Tjäderhane Leo,
Salo Tuula
Publication year - 2001
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.854
Subject(s) - collagenase , pathology , inflammation , matrix metalloproteinase , extracellular matrix , plasma cell , in situ hybridization , chemistry , interstitial collagenase , biology , medicine , immunology , bone marrow , microbiology and biotechnology , gene expression , enzyme , biochemistry , gene
Abstract Matrix metalloproteinases (MMPs) collectively degrade extracellular matrix and basement membrane proteins in chronic inflammation and bone‐destructive lesions. This study examined the ability of immunoglobulin‐producing plasma cells, typically present in sites of chronic inflammation, to express collagenases (MMP‐8 and ‐13) in vivo and in vitro . Phorbol‐12‐myristate‐13‐acetate, interleukin‐6, and tumour necrosis factor‐α and heparin with the tumour promoter or cytokines potently enhanced (up to nine‐fold) MMP‐8 and ‐13 expression by the RPMI 8226 myeloma cell line, as evidenced by western blotting and semi‐quantitative reverse transcriptase‐polymerase chain reaction. Immunohistochemical analysis and in situ hybridization revealed that plasma cells expressed MMP‐8 and ‐13 focally in periapical granulomas, odontogenic cysts, and malignant plasmacytomas. MMP‐8 and MMP‐13 from plasma cells can participate in bone organic matrix destruction at sites of chronic inflammation and neoplastic growth. Since MMP‐13 was more frequently expressed than MMP‐8 in plasma cells of strongly recurring keratocysts and malignant plasmacytomas, it is concluded that plasma cell MMP‐13 has a particularly important role in benign and malignant bone‐destructive lesions. Copyright © 2001 John Wiley & Sons, Ltd.