Human muscle-derived stem cells effective in animal models of incontinence

08/29/05

First human trials have started in Canada

MONTREAL, Aug. 31 Human muscle-derived cells, pluripotent stem cells found in muscle, have been used to cure stress urinary incontinence in animal models, a finding which signals that these cells are prime candidates to treat the condition in adults. The research will be presented by University of Pittsburgh researchers at the annual meeting of the International Continence Society Aug. 29 through Sept. 2 in Montreal.

In the study, the Pittsburgh researchers led by Michael Chancellor, M.D., injected the human muscle-derived stem cells into the periurethral muscle of a well-established animal model for stress urinary incontinence. After four weeks, the models' leak-point pressure, the pressure at which urine would leak from the bladder, had been restored to levels that would be seen normally.

"In past studies we have shown that muscle-derived cells from rats have been able to restore deficient muscle in the bladder. Using human muscle-derived cells was the next step in bringing this therapy to humans," said Dr. Chancellor, who is professor of urology at the University of Pittsburgh School of Medicine.

Researchers believe that the human muscle-derived cells were able to restore leak-point pressure to normal levels by differentiating into new muscle fibers, which prevented periurethral muscle atrophy. They will be returning to the lab to identify exactly how these cells work to regenerate muscle.

Clinical trials using muscle-derived cell therapy for incontinence have recently begun in Toronto.

Urinary incontinence affects 13 million Americans. Those with stress urinary incontinence involuntarily lose urine while doing activities that put stress on the abdomen, such as laughing, sneezing, coughing, lifting or walking. A result of damage to the urethral sphincter, stress incontinence is most often caused by childbirth, menopause or pelvic surgery.

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Last reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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