June 12, 2008 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.
Journal reference: Phosphorylation of GSK-3-beta by cGMP-dependent protein kinase II promotes hypertrophic differentiation of murine chondrocytes. Journal of Clinical Investigation. June 12, 2008
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