Effect of integrin β1 in the treatment of stress urinary incontinence by electrical stimulation.

The aim of the present study was to investigate the protective effect of integrin β1 in the treatment of stress urinary incontinence (SUI) by electrical stimulation, and the underlying mechanisms by which electrical stimulation regulates the collagen metabolism of female vaginal wall fibroblasts (FVWFs). FVWFs obtained from the vaginal wall tissue of patients with (Ingelman‑Sundberg scale; grade II, n=8; grade III, n=10) or without (n=8) SUI during gynecological operations were isolated by enzymatic digestion and subsequently identified by immunocytochemistry. Following this, cultured FVWFs were treated with an inhibitor of integrin β1, recombinant human integrin β1 and electrical stimulation (100 mv/mm, 2 h, 20 Hz), followed by total mRNA and protein extraction. mRNA and protein expression levels of integrin β1, transforming growth factor (TGF)‑β1 and collagen (COL) I and III in FVWFs were quantified by reverse transcription‑quantitative PCR (RT‑qPCR) and western blot analysis respectively. Integrin β1, TGF‑β1 and COL I and III expression levels were decreased in patients with SUI compared with healthy controls, and the grade III group had lower levels than the grade II group. Following electrical stimulation treatment, the expression levels of TGF‑β1, COL I and III were enhanced in the grade II group, but not in the grade III group. Nevertheless, the inhibitor of integrin β1 reduced the protective effect of electrical stimulation in the grade II group. In addition, electrical stimulation combined with recombinant human integrin β1 could also protect cells from SUI in the grade III group. The present study provides evidence for the increased degradation of the extracellular matrix and integrin β1 in the vaginal wall tissues of patients with SUI, and the protective effect of electrical stimulation against SUI via integrin β1. These results provide a novel mechanism for the treatment of SUI using electrical stimulation.