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JCI online early table of contents: June 12, 2008
Date:6/12/2008

E-mail: john.gribben@cancer.org.uk.

View the PDF of this article at: https://www.the-jci.org/article.php?id=35017


BONE BIOLOGY: How bone growth can be stunted in mice

Hiroshi Kawaguchi and colleagues, at the University of Tokyo, Japan, have provided new insight into the molecules that control the growth of the mouse skeleton.

Mice lacking a protein known as cGKII are dramatically smaller than mice expressing normal levels of this protein, because the bones of their legs and body are much shorter. In the study, it was found that the shorter bones were a result of a defect in bone growth, specifically in a process known as chondrocyte hypertrophy. Further analysis showed that in normal mouse chondrocytes, cGKII inhibited the function of a protein known as GSK-3-beta and that this was important for enhancing chondrocyte hypertrophy. In addition, the bone defects in mice lacking cGKII were partially rescued if the mice were engineered to express reduced levels of GSK-3-beta. These data indicate an important role for cGKII inhibition of GSK-3-beta function in skeletal growth and the authors are now investigating ways in which this information can be used to develop new therapeutics for skeletal disorders that result in dwarfism.

TITLE: Phosphorylation of GSK-3-beta by cGMP-dependent protein kinase II promotes hypertrophic differentiation of murine chondrocytes

AUTHOR CONTACT:
Hiroshi Kawaguchi
University of Tokyo, Tokyo, Japan.
Phone: 81-33815-5411 ext. 30473; Fax: 81-33818-4082; E-mail: kawaguchi-ort@h.u-tokyo.ac.jp.

View the PDF of this article at: https://www.the-jci.org/article.php?id=35243


METABOLIC DISEASE: FABP molecules help
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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