NF-kapaB activation in joint leads to cartilage destruction

Cartilage destruction is a hallmark feature of osteoarthritis. It is associated with elevated production of basic fibroblast growth factor (bFGF) and matrix metalloproteinase-13 (MMP-13). In addition, it is reported in the study briefly summarized below that the ability of cartilage to heal is severely limited in the presence of bFGF.

MMP-13 was found to be elevated in large part due to over-activation of NF-kB. This may in part account for the observation that cartilage healing is severely limited when joints are inflamed, but may progress rapidly once joint inflammation is relieved.

The publication:

October, 2007

Basic fibroblast growth factor activates the MAPK and NFkappaB pathways that converge on Elk-1 to control production of matrix metalloproteinase-13 by human adult articular chondrocytes.

Summary of the abstract

The pathology of joint destruction is associated with elevated production of basic fibroblast growth factor (bFGF) and matrix metalloproteinase-13 (MMP-13).

In osteoarthritic joint disease, expression of bFGF and MMP-13 in chondrocytes and their release into the synovial fluid are significantly increased.

We have previously found that the capacity for cartilage repair in human adult articular chondrocytes is severely compromised by minimal exposure to bFGF.

This study provides evidence that elevated expression of MMP-13 occurs through a pathway that includes activation of NF-kB, resulting in degradation of the cartilage matrix in degenerative joint diseases such as osteoarthritis.


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