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UT Southwestern Researchers Find Protein Transforms Sedentary Muscles To

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  • UT Southwestern Researchers Find Protein Transforms Sedentary Muscles To

    UT Southwestern Researchers Find Protein Transforms Sedentary Muscles To
    Resemble Exercised Muscles

    DALLAS - April 12, 2002 - A calcium-signaling protein transforms sedentary,
    easily fatigued muscles into energy-producing, fatigue-resistant muscles, UT
    Southwestern Medical Center at Dallas researchers report.
    In a study published in today's issue of Science, the researchers found that
    by genetically expressing the protein in skeletal muscles of laboratory mice,
    easily fatigued, or type II, muscle fibers were transformed into
    fatigue-resistant and mitochondria-rich, or energy-producing, type I muscle
    fibers, which resemble muscles that have been exercised.

    This research could lead to novel measures to stimulate muscles in patients
    with chronic diseases such as congestive heart failure or respiratory
    insufficiency, or individuals confined to bed rest.

    "The muscles of individuals who are on bed rest resemble type II muscle
    fibers; they fatigue quickly and the muscles are tired," said Dr. Rhonda
    Bassel-Duby, associate professor of internal medicine and co-author of the
    study. "If we have a way of mimicking this protein, we can convert the muscle
    with a drug to a more fatigue-resistant, mitochondria-rich muscle."

    Researchers expressed the active form of the calcium signaling protein called
    calcium/calmodulin-dependent protein kinase (CaMK) in the skeletal muscles of
    transgenic mice. CaMK controls production of mitochondria - structures in
    cells that are responsible for energy production - in mammalian muscle

    "Calcium signaling plays an essential role in muscle remodeling," said Dr.
    Hai Wu, lead author of the study and a postdoctoral research fellow in
    molecular biology.

    "CaMK has been intensely studied in neurons, where it is responsible for
    neuron plasticity and involved in learning and memory. Both neurons and
    muscle cells are excitable, and they share a lot of common signaling pathways
    in response to either brain activity or exercise," he said.

    Further studies will be conducted to determine the specific properties of
    CaMK responsible for these effects.

    "Greater understanding of the molecular-signaling pathways by which skeletal
    muscles sense and respond to changing activity patterns by altering gene
    expression ultimately may promote the development of novel measures to
    enhance the oxidative state of muscle, producing fatigue-resistant muscle,"
    Bassel-Duby said. "This could enhance muscle performance of patients
    overcoming muscle immobility or recovering from illnesses producing muscle
    fatigue such as heart failure."

    Other researchers involved in the study were Dr. Eiji Isotani, a visiting
    assistant professor in physiology; Dr. Shane Kanatous, a postdoctoral
    research fellow in internal medicine; Teresa Gallardo, a research scientist
    in cardiology; Dr. Frederick Thurmond, a postdoctoral research fellow in
    internal medicine; Dr. R. Sanders Williams, formerly chief of cardiology at
    UT Southwestern and presently dean of Duke University School of Medicine.

    The study was funded by grants from the National Institutes of Health.

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