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UCSF Researchers Identify Key Genes In Bone Healing Process That Could Lead To New, Molecular-Based Treatments

Anaheim, Calif. -- Researchers from the University of California San Francisco studying bone healing in animal models have found that two genes essential for bone formation in the fetus are also key to successful fracture repair in the adult.

Through a clever biologic regulatory process, the two genes become inactive when fetal development concludes but then resurface when needed to help mend broken bones.

"These findings shed new light on the bone formation process at the molecular level. Now we can use these principles to begin to develop new clinical treatments for troublesome fractures in which we mimic the natural healing process," said Theodore Miclau, MD, lead investigator and UCSF assistant professor of orthopaedic surgery who treats patients at San Francisco General Hospital Medical Center.

Miclau presented the study findings here today (February 5) at the annual meeting of the American Academy of Orthopaedic Surgeons. Working with adult mice, the UCSF team focused on the expression patterns of two embryonic genes, cbfal and Indian hedgehog, which are known to be indispensable in fetal bone formation.

Study results showed the genes reappeared in the bone of a mature animal when it underwent a fracture. During this process of "reinduction," the genes activated the expression of two proteins that contributed to bone healing in the adult model in a sequence very similar to the pattern that takes place during skeletal formation in the fetus.

The researchers analyzed bone tissue at the fracture site in adult mice at 3, 6, 8, 10, and 14 days after fracture to assess the presence of growth factors and other proteins. The UCSF team is believed to be the first to report the expression of the two genes in an animal bone repair model.

"Understanding this cascade of events and the specific growth factors involved in bone repair is a small step but a significant one. If we can replicate the pattern and target therapy directly to t
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Contact: Corinna Kaarlela
corinna@itsa.ucsf.edu
415-476-3804
University of California - San Francisco
5-Feb-1999


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