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- Matthew B. Greenblatt
- Department of Pathology, Division of Rheumatology, Allergy and Immunology,
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- Susan Y. Ritter
- Department of Medicine, and
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- John Wright
- Department of Orthopedics, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115;
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- Kelly Tsang
- Department of Medicine, and
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- Dorothy Hu
- Division of Endocrinology, Massachusetts General Hospital, Boston, MA 02114; and
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- Laurie H. Glimcher
- Weill Cornell Medical College, New York, NY 10065
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- Antonios O. Aliprantis
- Department of Medicine, and
説明
<jats:title>Significance</jats:title> <jats:p>Currently, little is understood about how the transcriptional regulation of cartilage breakdown contributes to pathogenesis of osteoarthritis (OA). Here, we report that, within cartilage, the transcription factor Nuclear factor of activated T cells c1 (NFATc1) displays selective expression in superficial articular chondrocytes. Accordingly, mice lacking both NFATc1 and NFATc2 in cartilage were generated and found to develop a severe, spontaneous and early-onset OA. These findings establish NFATc1 as a key transcriptional repressor of cartilage breakdown and OA. Additionally, these findings provide a unique model of OA that is an attractive platform for the preclinical development of treatments to alter the course of OA.</jats:p>
収録刊行物
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- Proceedings of the National Academy of Sciences
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Proceedings of the National Academy of Sciences 110 (49), 19914-19919, 2013-11-18
Proceedings of the National Academy of Sciences