Muscle cells enhance resistance to pro-inflammatory cytokine-induced cartilage destruction |
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Authors: | Dana M. Cairns Heenam Kwon Christopher R. Seufert Li Zeng |
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Affiliation: | a Program in Cellular, Molecular and Developmental Biology, Sackler School of Graduate Biomedical Sciences, Tufts University, 136 Harrison Avenue, Boston, MA 02111, USA b Department of Anatomy and Cellular Biology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA c Teachers and High School Students (TAHSS) Program, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA d Department of Orthopaedic Surgery, Tufts Medical Center, 800 Washington Street, Boston, MA 02111, USA |
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Abstract: | Pro-inflammatory cytokines IL-1β and TNFα 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-1β and TNFα. 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-1β and TNFα-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 NFκB, ESE-1, Cox-2, and GADD45β), 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. |
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Keywords: | Muscle Pro-inflammatory cytokines Cartilage Matrix |
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