Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 109, Issue 12, Pages E725-E733Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1120735109
Keywords
bone mass; T lymphocytes; bone cells
Categories
Funding
- National Institutes of Health [AR54625, AR49659]
- Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development [5I01BX000105]
- National Institute of Arthritis and Musculoskeletal and Skin Diseases [AR059364, AR056090, AR053607]
- National Institute on Aging [AG040013]
- Georgia Research Alliance
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Intermittent parathyroid hormone (iPTH) treatment stimulates T-cell production of the osteogenic Wnt ligand Wnt10b, a factor required for iPTH to activate Wnt signaling in osteoblasts and stimulate bone formation. However, it is unknown whether iPTH induces Wnt10b production and bone anabolism through direct activation of the parathyroid hormone (PTH)/PTH-related protein receptor (PPR) in T cells. Here, we show that conditional silencing of PPR in T cells blunts the capacity of iPTH to induce T-cell production of Wnt10b; activate Wnt signaling in osteoblasts; expand the osteoblastic pool; and increase bone turnover, bone mineral density, and trabecular bone volume. These findings demonstrate that direct PPR signaling in T cells plays an important role in PTH-induced bone anabolism by promoting T-cell production of Wnt10b and suggest that T cells may provide pharmacological targets for bone anabolism.
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