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JCI table of contents: May 24, 2010
Date:5/24/2010

TITLE: The antifibrotic effects of plasminogen activation occur via prostaglandin E2 synthesis in humans and mice

AUTHOR CONTACT:
Bethany B. Moore
University of Michigan, Ann Arbor, Michigan, USA.
Phone: 734.647.8378; Fax: 734.612.2331; E-mail: Bmoore@umich.edu.

Marc Peters-Golden
University of Michigan, Ann Arbor, Michigan, USA.
Phone: 734.763.9077; Fax: 734.764.4556; E-mail: petersm@umich.edu.

View this article at: http://www.jci.org/articles/view/38369?key=6eb0a308cb3d4624fa3c

BONE BIOLOGY: A key role in breaking bone down for the protein Cdc42


A team of researchers, led by Patrick Ross and Haibo Zhao, at Washington University School of Medicine, St. Louis, has determined that the protein Cdc42 has an important role in regulating the formation and function of cells that destroy bone in mice. Their data lead them to suggest that Cdc42 might be a good target for developing therapies for the treatment of conditions associated with bone loss such as osteoporosis.

Bone destruction is mediated by cells known as osteoclasts. Osteoporosis occurs when osteoclast numbers or function are greater than normal. In the study, mice lacking functional Cdc42 in their osteoclasts were resistant to bone loss in a model of postmenopausal osteoporosis. Conversely, mice in which Cdc42 activity was increased showed enhanced bone accumulation. Further analysis provided insight into the molecular mechanisms underlying the effects of Cdc42 and indicated that it had a key role in several signaling pathways that regulate osteoclast formation and function.

TITLE: Cdc42 regulates bone modeling and remodeling in mice by modulating RANKL/M-CSF signaling and osteoclast polarization

AUTHOR CONTACT:
F. Patrick Ross
Wash
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Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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