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Cell Transplants may Improve Severe Urinary Incontinence

by Medindia Content Team on November 13, 2007 at 1:36 PM
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Cell Transplants may Improve Severe Urinary Incontinence

Estimates are that up to 70 million people worldwide may be suffering from severe urinary incontinence. A major cause of urinary incontinence is a deficiency of the urethral sphincter muscle, often associated with trauma during child birth, resulting from prostate surgery, or due to aging.

According to a new study, those suffering from urethral sphincter muscle deficiency and resulting incontinence may eventually find relief through muscle cell transplants.

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Researchers publishing in the current issue of CELL TRANSPLANTATION (Vol. 16 No. 7) discovered that when skeletal myoblasts - progenitor muscle cells with the potential to develop into muscle fiber - were transplanted into female rats suffering from urethral sphincter deficiency, the transplanted muscle cells helped increase urethral pressure, improving incontinence.

"Self-renewing progenitor muscle cells can be cultivated in vitro," said Christophe Praud, PhD, of INSERM's Institut de Myologie, Universite Pierre et Marie Curie, Paris and lead author. "When grafted into normal striated skeletal muscle they fuse with host muscle fibers where they can form mosaic fibers or regenerate new fibers."
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In the double-blind study, self-donated (autologous) myoblast muscle cells were taken from the leg muscles of female laboratory rats and transplanted into their nerve-damaged and muscle-weakened sphincter muscles. A control group with the same urethral muscle deficiency received saline injections. When the grafted group was compared to the control group after 21 days, researchers found significant improvement in incontinence and measured near normal urethral closure pressures in the animals receiving the cell transplants.

"Our results suggest that implanting myoblasts could be a potential innovative therapy for urethral deficiencies that lead to human incontinence," concluded Praud.

Source: Eurekalert
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