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      IL-3 Decreases Cartilage Degeneration by Downregulating Matrix Metalloproteinases and Reduces Joint Destruction in Osteoarthritic Mice.

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          Abstract

          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.

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          Author and article information

          Journal
          J. Immunol.
          Journal of immunology (Baltimore, Md. : 1950)
          The American Association of Immunologists
          1550-6606
          0022-1767
          Jun 15 2016
          : 196
          : 12
          Affiliations
          [1 ] National Centre for Cell Science, Savitribai Phule Pune University Campus, Ganeshkhind, Pune 411007, India;
          [2 ] Department of Veterinary Surgery, Krantisinh Nana Patil College of Veterinary Science, Shirwal 412801, Satara, India;
          [3 ] Division of Endocrinology, Council of Scientific and Industrial Research-Central Drug Research Institute, Lucknow 226031, India; and.
          [4 ] Department of Orthopaedic Surgery, Armed Forces Medical College, Pune 411040, India.
          [5 ] National Centre for Cell Science, Savitribai Phule Pune University Campus, Ganeshkhind, Pune 411007, India; mohanwani@nccs.res.in.
          Article
          jimmunol.1500907
          10.4049/jimmunol.1500907
          27183574
          6a154491-b670-4d88-93f2-792bea9a428b
          History

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