Contribution of matrix metalloproteinase 2 to joint destruction in group BStreptococcus-induced murine arthritis

The role of matrix metalloproteinase-2 and matrix metalloproteinase-9 in antibody-induced arthritis.

Matrix metalloproteinases (MMPs) are a large group of enzymes responsible for matrix degradation. Among them, the family of gelatinases (MMP-2/gelatinase A and MMP-9/gelatinase B) is overproduced in the joints of patients with rheumatoid arthritis. Because of their degradative effects on the extracellular matrix, gelatinases have been believed to play an important role in progression and cartil...

Siglec15 Mediates Periarticular Bone Loss But Not Joint Destruction In Murine Antigen induced Arthritis

Expression of Matrix Metalloproteinase-2 and -9 in Meningioma

Background: Meningioma is one of the most common tumors of the central nervous system. It was shown that meningioma had up-regulated expression of Matrix Metalloproteinases (MMPs) that involved in cell growth, angiogenesis and metastasis.  Objectives: The aim of the study was the assessment of serum MMP-2 and -9 levels in patients with different grades of meningioma.  Materials & Me...

c-Jun N-terminal kinase is required for metalloproteinase expression and joint destruction in inflammatory arthritis.

Mitogen-activated protein kinase (MAPK) cascades are involved in inflammation and tissue destruction in rheumatoid arthritis (RA). In particular, c-Jun N-terminal kinase (JNK) is highly activated in RA fibroblast-like synoviocytes and synovium. However, defining the precise function of this kinase has been difficult because a selective JNK inhibitor has not been available. We now report the use...

Gene therapy in rheumatoid arthritis: how to target joint destruction?

Received: 7 September 1999 Revisions requested: 20 September 1999 Revisions received: 23 September 1999 Accepted: 23 September 1999 Published: 26 October 1999 © Current Science Ltd Important note about how to cite this article This article is also available online in the Arthritis Research website. To avoid confusion, please ensure that only the online version of the article is cited in any ref...