The two main areas of research in our laboratory are 1) the role of the central and peripheral sympathetic nervous system on bone remodeling and cancer metastasis and 2) the role of the RAS-GAP neurofibromin during skeleton development, growth, remodeling and repair.  

The skeleton is an organ that is richly supplied with blood vessels but also nerves. These nerves can be sensory (hence the pain when you hurt your bones) or  sympathetic. The latter type regulates body involuntary functions such as heart rate or breathing. Several studies within the last 10 years revealed the role of these nerves in regulating the process that maintains the skeleton in an optimal state in adulthood, i.e. bone remodeling. Our efforts now focus in identifying the pathophysiological relevance of these findings, using genetic and pharmacologic approaches.

The second main interest of the laboratory relates to the skeletal maladies observed in patients with neurofibromatosis type I (NF1). Tibia bowing, fracture non-union and dystrophic scoliosis are the most problematic skeletal conditions that can be found in some of these patients, and treatments are liited to invasive surgeries. We use our expertise in bone physiology and bone cell biology to understand the etiology of these skeletal conditions and to propose pre-clinical mouse models as well as targeted therapeutic approaches aiming at preventing or curing such conditions.



Featured publications

  1. Control of bone remodeling by the peripheral sympathetic nervous system. Elefteriou F, Campbell P, Ma Y (2014) Calcif Tissue Int 94(1): 140-51
    › Primary publication · 23765388 (PubMed) · PMC3883940 (PubMed Central)
  2. The ras-GTPase activity of neurofibromin restrains ERK-dependent FGFR signaling during endochondral bone formation. Ono K, Karolak MR, Ndong Jde L, Wang W, Yang X, Elefteriou F (2013) Hum Mol Genet 22(15): 3048-62
    › Primary publication · 23571107 (PubMed) · PMC3999379 (PubMed Central)
  3. Bone remodeling is regulated by inner ear vestibular signals. Vignaux G, Besnard S, Ndong J, Philoxène B, Denise P, Elefteriou F (2013) J Bone Miner Res 28(10): 2136-44
    › Primary publication · 23553797 (PubMed)
  4. Stimulation of host bone marrow stromal cells by sympathetic nerves promotes breast cancer bone metastasis in mice. Campbell JP, Karolak MR, Ma Y, Perrien DS, Masood-Campbell SK, Penner NL, Munoz SA, Zijlstra A, Yang X, Sterling JA, Elefteriou F (2012) PLoS Biol 10(7): e1001363
    › Primary publication · 22815651 (PubMed) · PMC3398959 (PubMed Central)

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Vanderbilt University Medical Center
2215 Garland Avenue
Room 1255D Light Hall
Nashville, TN 37232
615-322-7975 (p)

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Keywords & MeSH Terms

MeSH terms are retrieved from PubMed records. Learn more.

Key: MeSH Term Keyword

Adrenergic beta-Antagonists Bone Bone and Bones Bone Marrow Cells bone metastasis Bone Remodeling Cell Movement chondrocyte Chondrocytes Chondrogenesis Densitometry Extracellular Signal-Regulated MAP Kinases Female Gene Expression Humans Mammary Neoplasms, Experimental Mice Mice, Knockout Motor Activity osteoblast osteoclast Osteogenesis osteoporosis Rats, Sprague-Dawley Skeleton Sympathetic Nervous System Video Recording