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Vol. 12, Issue 12, 3852-3863, December 2001
and PTHrP Control Chondrocyte Proliferation by Activating
Cyclin D1 Expression
and
*Department of Biochemistry and Molecular Biology, University of
Calgary, Calgary, Alberta, Canada T2N 4N1; and
Exact coordination of growth plate chondrocyte proliferation
is necessary for normal endochondral bone development and growth. Here
we show that PTHrP and TGFDepartments of Developmental and Molecular Biology and
Medicine, Albert Einstein College of Medicine, Bronx, New York 10461
control chondrocyte cell cycle progression and proliferation by stimulating signaling pathways that
activate transcription from the cyclin D1 promoter. The TGF pathway
activates the transcription factor ATF-2, whereas PTHrP uses the
related transcription factor CREB, to stimulate cyclin D1 promoter
activity via the CRE promoter element. Inhibition of cyclin D1
expression with antisense oligonucleotides causes a delay in
progression of chondrocytes through the G1 phase of the cell cycle,
reduced E2F activity, and decreased proliferation. Growth plates from
cyclin D1-deficient mice display a smaller zone of proliferating
chondrocytes, confirming the requirement for cyclin D1 in chondrocyte
proliferation in vivo. These data identify the cyclin D1 gene as an
essential component of chondrocyte proliferation as well as a
fundamental target gene of TGF and PTHrP during skeletal growth.
Present address: CIHR Group in Skeletal Development
and Remodeling, Department of Physiology, University of Western
Ontario, London, Ontario, Canada.
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