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ShareJuly 6, 1999 — NEW BRUNSWICK/PISCATAWAY, N.J. -- Rutgers researchers David T. Denhardt and Susan R. Rittling, together with Hiroyuki Yoshitake and Masaki Noda of Tokyo Medical and Dental University, have announced new findings about a protein implicated in osteoporosis and metastatic cancer in the July 6 issue of the Proceedings of the National Academy of Sciences (PNAS).
Osteoporosis, one of the most common diseases affecting postmenopausal women, is a condition characterized by the progressive loss of bone density and thinning of bone tissue, resulting in increased fractures and diminished quality of life. In the United States, the number of patients is estimated at 12 million with an associated medical cost of about $1.2 billion.
The research explored the role of osteopontin (OPN), a protein produced by bone cells and regarded as functionally important in the regulation of bone metabolism. OPN is not required for normal bone development, but is required for certain types of bone remodeling and it strengthens the defenses of the body against certain forms of infection and injury. Considerable evidence also suggests that it facilitates the growth and spread (metastasis) of cancer cells. For this study, research methodology was designed to define more precisely the function of OPN and examine its effects on the onset of the bone resorption associated with osteoporosis.
"Susan Rittling, one of the co-authors and a research assistant professor at Rutgers, together with her colleagues developed a genetically altered strain of mice that lack the ability to produce OPN," said Denhardt, professor of cell biology and neuroscience with the Faculty of Arts and Sciences-New Brunswick. "Dr. Noda's group surgically removed the ovaries from mice of this strain to simulate the fall-off of estrogen production in postmenopausal women when their ovarian function decreases. When compared with a series of various control samples, we found that mice lacking OPN were significantly more resistant to the bone loss that accompanies estrogen depletion."
While no information exists regarding OPN deficiency in humans, the investigations of the Rutgers scientists and their colleagues present a compelling argument that some postmenopausal women might be expected to show enhanced resistance to osteoporosis because they possess an altered form of OPN.
"We propose that OPN is essential for postmenopausal osteoporosis," state the researchers in the PNAS paper. "Strategies to counteract OPN's action may prove effective in suppressing osteoporosis. Genetic analyses may predict certain patients who could have high or low risk of postmenopausal bone loss. New approaches would be available for the development of anti-bone-resorptive drugs, particularly those designed to suppress the action of OPN."
It follows that if the role of OPN in increasing cancer metastasis can be fully delineated, another subject under investigation by Denhardt and his laboratory group, the strategies to control the action of OPN will have implications for the treatment of cancer, as well.
Copies of the paper ("Osteopontin-Deficient Mice are Resistant to Ovariectomy-Induced Bone Resorption") are available to reporters from the PNAS news office by calling (202) 334-2138 or by e-mailing pnasnews@nas.edu.
NOTE TO REPORTERS/EDITORS: Additional information on David T. Denhardt's laboratory and its research can also be obtained at http:\lifesci.rutgers.edu/~denhardt/webpage.htm. He may also be reached for interviews by calling (732) 445-4569.
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