Elizabeth W. Bradley, Ph.D., studies diseases affecting the skeletal system, including osteoporosis and osteoarthritis (OA), and researches how associated tissues (such as bone and cartilage) are generated. Dr. Bradley's laboratory utilizes a combination of genetics, cell and molecular biology, and biochemistry.
She also employs a variety of preclinical models of disease such as surgical induction of joint instability and cortical bone defects to recapitulate disease processes. Through these combined approaches, Dr. Bradley hopes to identify new targets to slow degeneration and promote regeneration of skeletal tissues.
Osteoclasts are large, multinucleated cells that line bone surfaces and resorb bone. They arise via the fusion of myeloid progenitor cells and form long-lived syncytia within bone. Current projects in the lab are centered on limiting osteoclast-mediated bone resorption.
Research Interests
- Phosphatases in the skeletal system. Dr. Bradley and colleagues study how anabolic signaling is
dampened by phosphatases, a class of molecular switches, and how this affects skeletal generation, cartilage degeneration and bone resorption. Through this work, Dr. Bradley aims to identify novel therapeutic targets.
- Epigenetic control myeloid lineage cells. Dr. Bradley's lab studies how epigenetic factors, including histone deacetylases (Hdacs) regulate the differentiation of osteoclasts from myeloid linage cells and the impact on bone mass accrual and maintenance.
- The effects of progenitor cells age on bone loss and epigenetic programming of osteoclasts.
Advanced age and sex steroid deficiency are the largest predictors of osteoporosis in women, but itis unclear if post-menopausal bone loss and age-associated bone loss are driven by the same mechanisms.
