Effects of the decrease of β‐catenin expression on human vaginal fibroblasts of women with pelvic organ prolapse

Abstract

Background Pelvic organ prolapse (POP) lowers the quality of life in elderly women, and there have been no studies on its role in the pathogenesis of POP. The purpose of this study is to investigate the effect of β‐catenin on proliferation and collagen anabolism in human vaginal fibroblasts (HVFs). Materials and Methods The adherence and differential adherence methods were used to culture and purify HVFs. RNA interference was applied to knockdown β‐catenin and lithium chloride was used to activate Wnt/β‐catenin signaling pathway. β‐catenin nuclear translocation was tested by immunofluorescence, and HVF proliferation was detected by performing MTT assays. Results The expression of β‐catenin, phosphorylated‐β‐catenin, phosphorylated‐glycogen synthase kinase 3β (p‐GSK3β), collagen I, matrix metalloproteinase 2 (MMP2), and tissue‐derived inhibitors of metalloproteinases 2 (TIMP2) was assessed by western blot analysis. The expression of β‐catenin and collagen I was lower in HVFs of POP group than that of control group. The proliferation rate of HVFs in POP group was lower than that in control group. Knockdown of β‐catenin decreased the cell proliferation rate and the expression of collagen I. Lithium chloride can activate the Wnt/β‐catenin signaling pathway. Conclusion β‐catenin participates in the proliferation and collagen I synthesis of HVFs. The decrease of β‐catenin expression may be closely related to the occurrence, and development of POP. LiCl can activate the Wnt/β‐catenin signaling pathway in HVFs and thus increase HVFs proliferation and collagen synthesis.

FZD3 regulates the viability, apoptosis, and extracellular matrix degradation of vaginal wall fibroblasts in pelvic organ prolapse via the Wnt signaling pathway

“…[18] In this pathway, β-catenin regulates vaginal fibroblast proliferation and collagen synthesis, causing the development of POP. [30] Previous studies showed that FZD3 transduces Wnt signals and promotes the activation of the Wnt pathway. [16,31,32] Herein, we used IWP-4 to inactive the Wnt pathway.…”