Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 105, Issue 7, Pages 915-923Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI7039
Keywords
-
Categories
Funding
- NIAMS NIH HHS [R37 AR021707, R01 AR021707, AR44877, R56 AR044877, R01 AR044877, AR21707, R29 AR044877] Funding Source: Medline
- NIDCR NIH HHS [R37 DE004724, R01 DE004724, DE04724] Funding Source: Medline
Ask authors/readers for more resources
Bone continuously remodels in response to mechanical and physiological stresses, allowing vertebrates to renew bone as adults. Bone remodeling consists of the cycled synthesis and resorption of collagenous and noncollagenous extracellular matrix proteins, and an imbalance in this process can lead to disease states such as osteoporosis, or more rarely osteopetrosis. There is evidence that the extracellular matrix glycoprotein osteonectin or secreted protein acidic and rich in cysteine (BM-40) may be important in bone remodeling. Osteonectin is abundant in bone and is expressed in areas of active remodeling outside the skeleton. In vitro studies indicate that osteonectin can bind collagen and regulate angiogenesis, metalloproteinase expression, cell proliferation, and cell-matrix interactions. In some osteopenic states, such as osteogenesis imperfecta and selected animal models for bone fragility, osteonectin expression is decreased. To determine the function of osteonectin in bone, we used contact x-ray, histomorphometry and Northern blot analysis to characterize the skeletal phenotype of osteonectin-null mice. We found that osteonectin-null mice have decreased bone formation and decreased osteoblast and osteoclast surface and number, leading to decreased bone remodeling with a negative bone balance and causing profound osteopenia. These data indicate that osteonectin supports hone remodeling and the maintenance of bone mass in vertebrates.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available