Public Release: 

BMPs and bone loss: Get it through your noggin

JCI Journals

A study by Etsuko Abe and colleagues at Mount Sinai School of Medicine in New York has revealed that the balance between the expression of the bone-building protein BMP, and the BMP inhibitor noggin, plays a crucial role in regulating bone formation and loss. The overproduction of noggin may ultimately result in the net bone loss associated with conditions such as osteoporosis. The study suggests that recombinant BMP may prove useful in reversing age-related bone loss.

Bone morphogenetic proteins (BMPs) 2 and 4 are known to regulate hair follicle growth and skeletal development. These effects are inhibited by a protein called noggin, yet little was known about the role of noggin in the differentiation of bone-building cells (osteoblasts) and adult skeletal remodeling. In an article in the September 15 issue of the Journal of Clinical Investigation, Abe and colleagues have found that noggin is expressed in osteoblasts, chondrocytes, and macrophages. Infection of preosteoblastic cells with a retrovirus containing noggin inhibited osteoblast differentiation. A transgenic mouse that overexpressed noggin in mature osteoblasts displayed dramatic osteoporosis, decreased trabecular and calvarial bone, diminished bone formation rates, and reduced osteoblast differentiation.

These studies provide strong evidence that the balance between the expression of BMPs and noggin may determine the extent of bone building and breakdown, and ultimately bone mass in adult mice. The overproduction of noggin during aging may result in impaired bone building and function and hence, net bone loss.

Following the recent FDA approval of recombinant BMP2 for specific uses, there remains great clinical interest in the role of BMPs and noggin in the regulation of bone formation and repair in a variety of conditions, including osteoporosis. Abe and colleagues suggest that recombinant BMP may prove useful in reversing age-related bone loss.

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TITLE: Impaired osteoblastic differentiation, reduced bone formation, and severe osteoporosis in noggin-overexpressing mice

AUTHOR CONTACT:
Etsuko Abe
Mount Sinai School of Medicine, New York, New York, USA.
Phone: (212) 241-8735
Fax: (212) 534-4820
E-mail: etsuko.abe@mssm.edu

View the PDF of this article at: http://www.jci.org/cgi/content/full/112/6/924

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