A Protein that Helps Formation of Blood Vessels May Enrich Effectiveness of Incontinence Treatment

Stress urinary incontinence, the involuntary leakage of urine on exertion, sneezing or coughing, affects up to half of women with bladder control problems. It is often due to impaired function of the urinary sphincter, the circular muscle that controls the release of urine from the body.

Because of limitations of current therapies, scientists are exploring the possibility of injecting muscle cells into the sphincter to regenerate muscle tissue. This strategy involves isolation of immature cells found in the muscle tissue, called myoblasts, and growing them in the laboratory.

But because stress urinary incontinence primarily affects older women and men, an important question to consider is whether a patient’s age affects both the availability of myoblasts and the potential for muscle regeneration. In this first report to focus on these questions, scientists found that in mice, myoblasts could be isolated and expanded in sufficient quantities from mice ranging from 3 to 24 months of age. However, aging did impair the expansion capabilities of the cells as well as the function of the tissue that was engineered from them.

Because an important aspect of muscle development is a vascular network to supply nutrients and oxygen and to remove waste products from the tissue, the scientists wondered if increasing tissue vascularity would improve its function. They genetically engineered myoblasts to produce vascular endothelial growth factor (VEGF), a potent inducer of blood vessels.

They found that muscle tissue engineered with VEGF-expressing cells has a larger tissue mass and higher vascularity, as well as better contractility, suggesting that the results may have future therapeutic applications for stress urinary incontinence in older women.

(Angiogenic gene modification of skeletal muscle cells to compensate for ageing-induced decline in bioengineered functional muscle tissue. Delo DM, Eberli D, Williams JK, Andersson KE, Atala A, Soker S. BJU Int. 2008 Sep;102(7):878-84. Epub 2008 May 16.