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Plasma matrix metalloproteinase and tissue inhibitor of metalloproteinase in patients with agnogenic myeloid metaplasia or idiopathic primary myelofibrosis
Author(s) -
Wang Jen C.,
Novetsky Akiva,
Chen Chi,
Novetsky Allan D.
Publication year - 2002
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.2002.03874.x
Subject(s) - myelofibrosis , matrix metalloproteinase , medicine , fibrosis , metaplasia , essential thrombocythemia , pathology , extracellular matrix , bone marrow , myeloid , polycythemia vera , biology , microbiology and biotechnology
Summary. Agnogenic myeloid metaplasia (AMM) is characterized by bone marrow fibrosis with abnormal accumulation of extracellular matrix components (ECM), which is dependent on the balance between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). Twenty‐five patients with AMM, 30 with essential thrombocythemia (ET), 12 with polycythemia vera (PV) and 20 normal control subjects were studied. AMM patients had decreased plasma levels of MMP‐3 and marked elevated levels of TIMP‐1, but MMP‐1, MMP‐2 and MMP‐9 levels were not significantly different from control subjects. Elevated levels of plasma TIMP‐1, but not MMPs, were found in ET and PV. Reduced MMP activity together with increased TIMP‐1 activity may be essential in fibrosis formation.