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Myoblasts differentiated from adipose-derived stem cells to treat stress urinary incontinence.
Urology 2010 March
OBJECTIVES: To investigate the application of adipose-derived stem cell (ADSC) technology in the treatment of stress incontinence.
METHODS: The vaginal balloon dilatation method was used to establish an animal model of stress incontinence (in 20 female Sprague-Dawley rats), which was further examined by urodynamics and histology. Endogenous rat ADSCs were collected and induced into myoblasts with 5-Aza induction technology in vitro. The identity of myoblasts was confirmed through immunofluorescence labeling with desmin and myosin. Induced cells were injected into the posterior urethral muscularis in the bladder neck of animals with stress incontinence. The effects were examined after 1 and 3 months by urodynamics and histology. Untreated ADSCs were also implanted as a method of control.
RESULTS: Both maximal bladder capacity and leak point pressure significantly increased after 1 and 3 months postimplantation, compared with the control (P <.05). Increased thickness of inferior muscularis in urethral mucosa and a greater number of large longitudinal muscle bundles were observed. Increased numbers of myoblasts appeared under the mucosa, as demonstrated by the immunochemistry analysis of alpha-smooth actin.
CONCLUSIONS: ADSCs have the ability of differentiating into multiple lineages, including myoblasts. This ability to induce myoblasts can be used to treat stress incontinence, with the advantages of minimal invasion and faster recovery.
METHODS: The vaginal balloon dilatation method was used to establish an animal model of stress incontinence (in 20 female Sprague-Dawley rats), which was further examined by urodynamics and histology. Endogenous rat ADSCs were collected and induced into myoblasts with 5-Aza induction technology in vitro. The identity of myoblasts was confirmed through immunofluorescence labeling with desmin and myosin. Induced cells were injected into the posterior urethral muscularis in the bladder neck of animals with stress incontinence. The effects were examined after 1 and 3 months by urodynamics and histology. Untreated ADSCs were also implanted as a method of control.
RESULTS: Both maximal bladder capacity and leak point pressure significantly increased after 1 and 3 months postimplantation, compared with the control (P <.05). Increased thickness of inferior muscularis in urethral mucosa and a greater number of large longitudinal muscle bundles were observed. Increased numbers of myoblasts appeared under the mucosa, as demonstrated by the immunochemistry analysis of alpha-smooth actin.
CONCLUSIONS: ADSCs have the ability of differentiating into multiple lineages, including myoblasts. This ability to induce myoblasts can be used to treat stress incontinence, with the advantages of minimal invasion and faster recovery.
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