Plasma matrix metalloproteinase and tissue inhibitor of metalloproteinase in patients with agnogenic myeloid metaplasia or idiopathic primary myelofibrosis

Jen C. Wang, Akiva Novetsky, Chi Chen, Allan D. Novetsky

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)709-712
Number of pages4
JournalBritish Journal of Haematology
Volume119
Issue number3
DOIs
StatePublished - 2002

Fingerprint

Tissue Inhibitor of Metalloproteinases
Primary Myelofibrosis
Matrix Metalloproteinase Inhibitors
Tissue Inhibitor of Metalloproteinase-1
Essential Thrombocythemia
Polycythemia Vera
Matrix Metalloproteinases
Matrix Metalloproteinase 3
Matrix Metalloproteinase 1
Matrix Metalloproteinase 2
Matrix Metalloproteinase 9
Extracellular Matrix
Fibrosis

Keywords

  • Agnogenic myeloid metaplasia
  • Idiopathic primary myelofibrosis
  • Matrix metalloproteinase
  • Tissue inhibitor of metalloproteinase

ASJC Scopus subject areas

  • Hematology

Cite this

Plasma matrix metalloproteinase and tissue inhibitor of metalloproteinase in patients with agnogenic myeloid metaplasia or idiopathic primary myelofibrosis. / Wang, Jen C.; Novetsky, Akiva; Chen, Chi; Novetsky, Allan D.

In: British Journal of Haematology, Vol. 119, No. 3, 2002, p. 709-712.

Research output: Contribution to journalArticle

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