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Kour , S. and Garimella , M.G. and Shiroor , D.A. and Mhaske , S.T. and Joshi , S.R. and Singh , K. and Pal , S. and Mittal , M. and Krishnan , H.B. and Chattopadhyay, N. and Ulemale , A.H. and Wani , M.R. (2016) IL-3 Decreases Cartilage Degeneration by Downregulating Matrix Metalloproteinases and Reduces Joint Destruction in Osteoarthritic Mice. Journal of Immunology , 196 (12). pp. 5024-5035.

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Osteoarthritis (OA) is a chronic disease of articular joints that leads to degeneration of both cartilage and subchondral bone. These degenerative changes are further aggravated by proinflammatory cytokines including IL-1β and TNF-α. Previously, we have reported that IL-3, a cytokine secreted by activated T cells, protects cartilage and bone damage in murine models of inflammatory and rheumatoid arthritis. However, how IL-3 protects cartilage degeneration is not yet known. In this study, we investigated the role of IL-3 on cartilage degeneration under both in vitro and in vivo conditions. We found that both mouse and human chondrocytes show strong expression of IL-3R at gene and protein levels. IL-3 increases the expression of mouse chondrocyte-specific genes, Sox9 and collagen type IIa, which were downregulated by IL-1β. Moreover, IL-3 downregulated IL-1β– and TNF-α–induced expression of matrix metalloproteinases in both mouse and human chondrocytes. Interestingly, IL-3 reduces the degeneration of articular cartilage and subchondral bone microarchitecture in a mouse model of human OA. Moreover, IL-3 showed the preventive and therapeutic effects on cartilage degeneration induced by IL-1β in micromass pellet cultures of human mesenchymal stem cells. Thus, to our knowledge, we provide the first evidence that IL-3 has therapeutic potential in amelioration of degeneration of articular cartilage and subchondral bone microarchitecture associated with OA.

Item Type: Article
Subjects: Infection and Immunity
Depositing User: Mr. Rameshwar Nema
Date Deposited: 01 Jul 2016 04:04
Last Modified: 01 Jul 2016 04:04
URI: http://nccs.sciencecentral.in/id/eprint/290

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