Elizabeth Bradley, PhD

Assistant Professor, Department of Orthopedic Surgery

Elizabeth Bradley

Contact Info

[email protected]

Office Phone 612-301-2810

Office Address:
2-212 MTRF
2001 6th Street SW
Minneapolis, MN 55455

PhD, Biomedical Sciences, Biochemistry and Molecular Biology, Mayo Clinic

BS, Cell Biology, University of Minnesota, Duluth


Musculoskeletal problems are one of the leading reasons for physician visits each year.  As such, diseases such as osteoporosis and osteoarthritis impart a major social and economic burden and are associated with significant morbidity and mortality.  This burden will grow as the population ages, unless treatment modalities are expanded.  The ultimate goal of Dr. Bradley's research is to provide a better understanding of skeletal generation and degeneration, and to identify new therapeutic approaches.


bone cell biology, mouse genetics, osteoporosis, osteoarthritis, myeloid lineage cells.

Awards & Recognition

John Haddad Young Investigator Award, Advances in Mineral Metabolism, 2011
F32 Ruth L. Kirschstein National Service Award (NRSA) NIH, 2011-2013
K01 Career Development Award, NIH, 2014-2019
American Society for Bone and Mineral Research Mid-CareerAward, 2019

Professional Associations

Member, American Society for Bone and Mineral Research
Member, Orthopedic Research Society
Member, American Society of Biochemistry and Molecular Biology
Associate Editor, BMC Musculoskeletal Disorders
Editorial Board, Journal of Bone and Mineral Research


Research Summary/Interests

Elizabeth W. Bradley, PhD 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 synticia within bone.  Current projects in the lab are centered on limiting osteoclast-mediated bone resorption.

  • 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 lineage 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 it is unclear if post-menopausal bone loss and age-associated bone loss are driven by the same mechanisms.


  • Molstad DHH, Meyer MR, Norton A. Westendorf JJ, Mansky KK, and Bradley, EW.  Macrophage lineage Hdac3 Depletion Enhances Bone Healing and Limits Osteoclast Fusion via Pmepa1. Scientific Reports. 2020
  • Mattson AM, Begun DL, Molstad DHH, Meyer MA, Oursler MJ, Westendorf JJ, Bradley, EW.  Deficiency in the phosphatase PHLPP1 suppresses osteoclast-mediated bone resorption and enhances bone formation in mice.  J Biol. Chem. 2019
  • Castillejo Becerra CM, Mattson AM, Molstad DHH, Lorang IM, Westendorf JJ,  Bradley, EW.  DNA Methylation and FoxO3a regulate Phlpp1 expression in chondrocytes. J Cell Biochem. 2018 May 18.  
  • Carpio LR, Bradley EW, McGee-Lawrence ME, Weivoda MM, Poston DD, Dudakovic A, Xu M, Tchkonia T. Kirkland JL, van Wijnen AJ, Oursler MJ, Westendorf JJ, Histone deacetylase 3 supports endochondral bone formation by controlling cytokine signaling and matrix remodeling. Sci Signal. 2016. Aug 9;9(440).
  • Fang D, Han J, Gan H, Lee JH, Jin L, Wang Z, Zhou H, Riester SM, Wang J, Yang N, Bradley, EW, Ho T, Rubin BP, Bridge JA, van Wijnen A, Oliveira A, Xu RM, Westendorf JJ, Zhang Z. The histone H3.3K36M mutation reprograms in the epigenome of chondroblastomas. Science, 2016. 352(6291):1344-8. PMCID:PMC5460624
  • Bradley EW, Carpio LR, McGee-Lawrence ME, Castellejo Becerra C, Amanatullah DF, Ta LE, Otero M, Goldring MB, Kakar S, Westendorf JJ. Phlpp1 facilitates post-traumatic osteoarthritis and is induced by inflammation and promoter demethylation in human osteoarthritis.  Osteoarthritis Cartilage, 24(6): 1021-8; 2016.  PMCID: PMC4875839
  • Xu M, Bradley EW, Weivoda MM, Hwang SM, Pirtskhalava T, Decklever T, Curran GL, Ogrodnik M, Jurk D, Johnson KO, Lowe V, Tchkonia T. Westendorf JJ, Kirkland JL. Transplanted senescent cells induced an osteoarthritis-like condition in mice.  J. Gerntol A Biol Sci Med Sci, 2016 Aug 10. pil: glw154.