Barton is a molecular physiologist with a primary interest in skeletal muscle repair. Her work has broad applications including accelerating the resolution of muscle damage after acute injuries, altering the balance between damage and repair in chronic injury associated with neuromuscular disease, and enhancing the repair axis in aging muscle. She has spent the last 20 years studying insulin-like growth factor I (IGF-I), a key player in the muscle regeneration process. More recently, Barton has focused on how muscles sense load, and how these sensors become dysfunctional in muscle disease. Her research has been supported by grants from NIH, NASA, Muscular Dystrophy Association, and the DOD.
Industry Expertise (2)
Health and Wellness
Areas of Expertise (5)
Skeletal Muscle Repair
Mechanical Signal Transduction
Optimization of IGF-I for Muscle Therapeutics
Viral Gene Therapy
Media Appearances (2)
Promising New Strategy to Help Broken Bones Heal Faster
Laboratory Equipment online
From earlier work focused on muscular dystrophy conducted with former Penn Dental Medicine faculty member Elizabeth Barton, now at the University of Florida, the researchers believed that a particular form of IGF, a precursor of the protein that includes a separate component known as an e-peptide, was likely to stimulate regeneration better than mature IGF-1 that lacked the peptide. Current IGF1 used in the clinic not only lacks the e-peptide but is also glycosylated, a less active form.
In space, not all muscles are created equal
UF News online
Muscles waste away when they’re not used, right? Turns out, it’s not that simple. Elisabeth Barton, a physiology professor in the University of Florida College of Health and Human Performance, studies how muscles react to reduced load. Her latest discovery comes from an unlikely source: mice in space.
Increased collagen cross-linking is a signature of dystrophin-deficient muscleMuscle & Nerve
Collagen cross-linking is a key parameter in extracellular matrix (ECM) maturation, turnover, and stiffness. We examined aspects of collagen cross-linking in dystrophin-deficient murine, canine, and human skeletal muscle.
Muscle hypertrophy induced by myostatin inhibition accelerates degeneration in dysferlinopathyHuman Molecular Genetics
Myostatin is a secreted signaling molecule that normally acts to limit muscle growth. As a result, there is extensive effort directed at developing drugs capable of targeting myostatin to treat patients with muscle loss. One potential concern with this therapeutic approach in patients with muscle degenerative diseases like muscular dystrophy is that inducing hypertrophy may increase stress on dystrophic fibers, thereby accelerating disease progression.
Selective Retinoic Acid Receptor γ Agonists Promote Repair of Injured Skeletal Muscle in MouseThe American Journal of Pathology
Retinoic acid signaling regulates several biological events, including myogenesis. We previously found that retinoic acid receptor γ (RARγ) agonist blocks heterotopic ossification, a pathological bone formation that mostly occurs in the skeletal muscle. Interestingly, RARγ agonist also weakened deterioration of muscle architecture adjacent to the heterotopic ossification lesion, suggesting that RARγ agonist may oppose skeletal muscle damage.
Masticatory muscles of mouse do not undergo atrophy in spaceThe FASEB Journal
Muscle loading is important for maintaining muscle mass; when load is removed, atrophy is inevitable. However, in clinical situations such as critical care myopathy, masticatory muscles do not lose mass. Thus, their properties may be harnessed to preserve mass. We compared masticatory and appendicular muscles responses to microgravity, using mice aboard the space shuttle Space Transportation System-135. Age- and sex-matched controls remained on the ground. After 13 days of space flight, 1 masseter (MA) and tibialis anterior (TA) were frozen rapidly for biochemical and functional measurements, and the contralateral MA was processed for morphologic measurements.
Gamma-sarcoglycan is required for the response of archvillin to mechanical stimulation in skeletal muscleHuman Molecular Genetics
Loss of gamma-sarcoglycan (γ-SG) induces muscle degeneration and signaling defects in response to mechanical load, and its absence is common to both Duchenne and limb girdle muscular dystrophies. Growing evidence suggests that aberrant signaling contributes to the disease pathology; however, the mechanisms of γ-SG-mediated mechanical signaling are poorly understood. To uncover γ-SG signaling pathway components, we performed yeast two-hybrid screens and identified the muscle-specific protein archvillin as a γ-SG and dystrophin interacting protein.
- American Society for Cell Biology : Member
- American Physiological Society : Member
- Biophysical Society : Member