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View Full Version : 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



Steve Cowin
09-21-2004, 11:13 AM
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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