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  • 1
    Publication Date: 2007-01-27
    Description: The normal synovium forms a membrane at the edges of joints and provides lubrication and nutrients for the cartilage. In rheumatoid arthritis, the synovium is the site of inflammation, and it participates in an organized tissue response that damages cartilage and bone. We identified cadherin-11 as essential for the development of the synovium. Cadherin-11-deficient mice have a hypoplastic synovial lining, display a disorganized synovial reaction to inflammation, and are resistant to inflammatory arthritis. Cadherin-11 therapeutics prevent and reduce arthritis in mouse models. Thus, synovial cadherin-11 determines the behavior of synovial cells in their proinflammatory and destructive tissue response in inflammatory arthritis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, David M -- Kiener, Hans P -- Agarwal, Sandeep K -- Noss, Erika H -- Watts, Gerald F M -- Chisaka, Osamu -- Takeichi, Masatoshi -- Brenner, Michael B -- K08 AR2214/AR/NIAMS NIH HHS/ -- R01 AR48114/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Feb 16;315(5814):1006-10. Epub 2007 Jan 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine and Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard Medical School, 1 Jimmy Fund Way, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17255475" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/therapeutic use ; Arthritis, Experimental ; Arthritis, Rheumatoid/metabolism/*pathology/therapy ; Cadherins/*antagonists & inhibitors/biosynthesis/deficiency/*physiology ; Cell Adhesion/physiology ; Disease Models, Animal ; Extracellular Matrix/metabolism ; Fibroblasts/metabolism ; L Cells (Cell Line) ; Male ; Mice ; Mice, Inbred C57BL ; Organ Culture Techniques ; Synovial Membrane/*cytology/*pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2010-01-30
    Description: In addition to their pivotal role in thrombosis and wound repair, platelets participate in inflammatory responses. We investigated the role of platelets in the autoimmune disease rheumatoid arthritis. We identified platelet microparticles--submicrometer vesicles elaborated by activated platelets--in joint fluid from patients with rheumatoid arthritis and other forms of inflammatory arthritis, but not in joint fluid from patients with osteoarthritis. Platelet microparticles were proinflammatory, eliciting cytokine responses from synovial fibroblasts via interleukin-1. Consistent with these findings, depletion of platelets attenuated murine inflammatory arthritis. Using both pharmacologic and genetic approaches, we identified the collagen receptor glycoprotein VI as a key trigger for platelet microparticle generation in arthritis pathophysiology. Thus, these findings demonstrate a previously unappreciated role for platelets and their activation-induced microparticles in inflammatory joint diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2927861/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2927861/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boilard, Eric -- Nigrovic, Peter A -- Larabee, Katherine -- Watts, Gerald F M -- Coblyn, Jonathan S -- Weinblatt, Michael E -- Massarotti, Elena M -- Remold-O'Donnell, Eileen -- Farndale, Richard W -- Ware, Jerry -- Lee, David M -- G0500707/Medical Research Council/United Kingdom -- HL091269/HL/NHLBI NIH HHS/ -- HL50545/HL/NHLBI NIH HHS/ -- K08AR051321/AR/NIAMS NIH HHS/ -- P01 AI065858/AI/NIAID NIH HHS/ -- R01 HL050545/HL/NHLBI NIH HHS/ -- R01 HL050545-16/HL/NHLBI NIH HHS/ -- R01 HL050545-18/HL/NHLBI NIH HHS/ -- R21 HL091269/HL/NHLBI NIH HHS/ -- R21 HL091269-01A2/HL/NHLBI NIH HHS/ -- RG/09/003/27122/British Heart Foundation/United Kingdom -- British Heart Foundation/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jan 29;327(5965):580-3. doi: 10.1126/science.1181928.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20110505" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/blood/immunology ; Arthritis, Rheumatoid/*blood/*immunology/physiopathology ; Blood Platelets/cytology/*physiology/ultrastructure ; Cell-Derived Microparticles/metabolism/*physiology ; Cells, Cultured ; Collagen/*metabolism ; Cytokines/*metabolism ; Extracellular Matrix/metabolism ; Fibroblasts/immunology/metabolism ; Humans ; Interleukin-1/metabolism ; Mice ; Mice, Transgenic ; Platelet Activation ; Platelet Membrane Glycoproteins/metabolism ; Receptors, Collagen/metabolism ; Synovial Fluid/cytology/*immunology ; Synovial Membrane/cytology/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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