|
 |
|||||||||||||||||||
|
|||||||||||||||||||
|
|||||||||||||||||||
 |
 |
|
|
a Department of Physiology and Biophysics, UMDNJ-Robert Wood Johnson Medical School, Piscataway, New Jersey, USA b Departments of Orthopedic Surgery and Molecular Biology and Biochemistry, Mayo Clinic, Rochester, Minnesota, USA
Key Words: histone deacetylases • parathyroid hormone • osteoblasts
Address for correspondence: Nicola C. Partridge, Department of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, 675 Hoes Lane, Piscataway, New Jersey 08854. Voice: 732-235-4552; fax: 732-235-3977. partrinc{at}umdnj.edu
Parathyroid hormone (PTH) functions as an essential regulator of calcium homeostasis and as a mediator of bone remodeling. We have already shown that PTH stimulates the expression of matrix metalloproteinase-13 (MMP-13), which is responsible for degrading components of extracellular matrix. We have hypothesized that histone deacetylases (HDACs) are involved with PTH-induced MMP-13 gene expression in the osteoblastic cell line, UMR 106–01. We have shown that PTH profoundly regulates HDAC4 in UMR 106–01 cells through a PKA-dependent pathway, leading to removal of HDAC4 from the MMP-13 promoter and its enhanced transcription. Understanding the mechanism of how HDACs affect osteoblast differentiation and mineralization will identify new theraupeutic methods for bone diseases, such as osteoporosis and multiple myeloma.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
 |
 |
