muscle and athritis

Biochem Biophys Res Commun. 2009 Dec 28. [Epub ahead of print]

Muscle cells enhance resistance to pro-inflammatory cytokine-induced cartilage destruction.
Cairns DM, Uchimura T, Kwon H, Lee PG, Seufert CR, Matzkin E, Zeng L.

Program in Cellular, Molecular and Developmental Biology, Sackler School of Graduate Biomedical Sciences, Tufts University, 136 Harrison Avenue, Boston, MA 02111, USA.

Pro-inflammatory cytokines IL-1beta and TNFalpha play important roles in the manifestation of arthritis by disrupting the anabolic and catabolic activities of the chondrocytes. We observed a novel mechanism of cartilage regulation by which muscle cells diminish the response of chondrocytes to IL-1beta and TNFalpha. We found that chondrocytes cocultured with muscle cells or cultured in muscle cell-conditioned medium significantly enhanced the expression of cartilage matrix proteins (collagen II and collagen IX) and resisted IL-1beta and TNFalpha-induced cartilage damage. Our data suggest that this effect is achieved by inhibiting the expression of key components of the signaling pathways of pro-inflammatory cytokines (including NFkappaB, ESE-1, Cox-2 and GADD45beta, leading to attenuated expression of cartilage degrading enzymes (MMPs and ADAMTS4). Therefore, our work unveils a potential role of muscle in regulating cartilage homeostasis and response to pro-inflammatory stimuli, and provides insights on designing treatment strategies for joint degenerative diseases such as arthritis. Copyright © 2009. Published by Elsevier Inc.