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NYC Bone Seminar on Tuesday,September 28th: David Denhardt on Osteopontin,a Cytokine and Bone Matrix Protein, Augments Bone Remodeling,Metastasis, and Autoimmune Disease Progression

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  • NYC Bone Seminar on Tuesday,September 28th: David Denhardt on Osteopontin,a Cytokine and Bone Matrix Protein, Augments Bone Remodeling,Metastasis, and Autoimmune Disease Progression

    Dear colleagues and students:

    The Fall 2004 Bone Seminar Series kicks off on Tuesday September 28
    with a presentation by David T. Denhardt PhD of Rutgers University,
    who will speak on "Osteopontin, a Cytokine and Bone Matrix Protein,
    Augments Bone Remodeling, Metastasis, and Autoimmune Disease
    Progression."

    Details of all seminars appear on our website: http://bonenet.net/index.html
    Details of this seminar also appear below.

    I would greatly appreciate in any person interested in the Bone
    Seminar Series, the Bone Fluid Flow Workshops or the BoneNet.net
    website http://bonenet.net, filling out a questionnaire to help me
    prepare the annual report to the National Science Foundation, which
    supports these activities. The questionnaire is also downloadable at
    http://bonenet.net/questionnaire_0409.pdf.

    Many thanks, Steve Cowin

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    September 28, 2004 Seminar

    SPEAKER: David T. Denhardt PhD, Department of Cell Biology and
    Neuroscience, Rutgers University, Piscataway Campus

    TOPIC: Osteopontin, a Cytokine and Bone Matrix Protein, Augments Bone
    Remodeling, Metastasis, and Autoimmune Disease Progression

    PLACE AND TIME: Room 9204, CUNY Graduate Center, 7:00 PM

    ABSTRACT: Osteopontin (OPN) is a phosphorylated, glycosylated protein
    found not only extracellularly in all body fluids and in mineralized
    matrices but also intracellularly at the cytoskeletal/plasma membrane
    interface. The extracellular form is capable of engaging some
    half-dozen integrins and at least two CD44 variants. OPN signaling
    regulates gene expression (e.g., iNOS expression induced by
    endotoxin) and cell motility, stimulating a chemotactic response. It
    enhances the survival of cells exposed to various stresses by
    inhibiting apoptosis. OPN can stimulate tumor cell metastasis and the
    progression of autoimmune disease: Mice lacking OPN are less
    susceptible to arthritis induced by anti-type II collagen antibodies
    (Noda) and to experimental autoimmune encephalomyelitis induced by
    myelin oligodendrocyte glycoprotein peptides (Steinman, Cantor). They
    are also unable to remodel bone in response to various stresses
    (ovariectomy, hind-limb suspension), possibly in part because OPN is
    required for normal osteoclast function (Hruska, Noda, Sodek).

    RESEARCH INTERESTS of Dave Denhardt: His research interests currently
    focus on the systems physiology of OPN and TIMP-1 (tissue inhibitor
    of metalloproteinases-1). Both in different ways stimulate tumor cell
    metastasis and he would like to know why. With respect to OPN, he
    would like to understand how it functions in such apparently diverse
    processes as bone remodeling and autoimmune disease.

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    Questions and Feedback Contact

    Stephen C. Cowin PhD
    New York Center for Biomedical Engineering
    Departments of Biomedical and Mechanical Engineering
    School of Engineering
    The City College of New York
    138th Street and Convent Avenue
    New York, NY 10031-9198, USA

    Phone:
    (212) 799-7970 (Office at Home)
    (212) 650-5208 (Office at Work)

    Fax:
    (212) 799-7970 (Office at Home)

    Email:
    scowin@earthlink.net

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