Silencing of cysteine and serine rich nuclear protein 1 inhibits apoptosis, senescence and collagen degradation in human-derived vaginal fibroblasts in response to oxidative stress or DNA damage.

Pelvic organ prolapse (POP) is a group of diseases caused by extracellular matrix (ECM) degradation in pelvic supportive tissues. Cysteine and serine rich nuclear protein 1 (CSRNP1) is involved in cell proliferation and survival regulation, and reportedly facilitates collagen breakdown in human chondrocytes. The present study aimed to probe the effect of CSRNP1 on collagen metabolism in human-derived vaginal fibroblasts. High expression of CSRNP1 was found in POP patient-derived vaginal fibroblasts in comparison to normal-derived vaginal fibroblasts. Following functional experiments revealed that CSRNP1 overexpression led to proliferation inhibition, apoptosis and collagen degradation in normal vaginal fibroblasts. In line with this, silencing of CSRNP1 inhibited hydrogen peroxide (H2O2)-triggered apoptosis, ROS generation and collagen loss in normal vaginal fibroblasts. Silencing of CSRNP1 also reduced the expression of cell senescence markers p21 and γ-H2Ax (the histone H2Ax phosphorylated at Ser139), as well as curbed collagen breakdown in normal vaginal fibroblasts caused by a DNA damage agent etoposide. Transcriptomic analysis of vaginal fibroblasts showed that differentially expressed genes affected by CSRNP1 overexpression were mainly enriched in the Wnt signaling pathway. Treatment with a Wnt pathway inhibitor DKK1 blocked CSRNP1 knockdown-caused collagen deposition. Mechanistically, CSRNP1 was identified to be a target of Snail family transcriptional repressor 2 (SNAI2). Forced expression of CSRNP1 reversed the anti-apoptotic, anti-senescent and anti-collagen loss effects of SNAI2 in normal vaginal fibroblasts exposed to H2O2 or etoposide. Our study indicates that the SNAI2/CSRNP1 axis may be a key driver in POP progression, which provides a potential therapeutic strategy for POP.

Analysis of clinical interventional strategy for women with urinary incontinence complicated with diabetes mellitus.

INTRODUCTION AND HYPOTHESIS: This study aims to investigate clinical therapeutic measures for women with urinary incontinence (UI) complicated with diabetes mellitus (DM). METHODS: We performed a retrospective cohort study, including 462 female patients with UI complicated with DM (group A) and 901 patients with UI without DM (group B). Both A and B groups were divided into three subgroups according to their UI types (pure stress UI, mixed UI dominated by urge UI, and by overactive bladder syndrome) and received corresponding treatments. The subjective and objective effective rates were analyzed statistically. RESULTS: The overall subjective effective rates were 62.99% and 85.23% and the overall objective effective rates were 67.53% and 87.24% for groups A and groups B, respectively; the subjective and objective effective rates were 73.68% and 89.47% for group A1 (patients with pure stress UI in group A). There was no statistical difference in group A1 between subjective and objective effective rates. CONCLUSION: Unsatisfactory clinical therapeutic efficacy was observed in women with UI complicated with DM; surgical operation should be deliberated cautiously for women with SUI complicated with DM.

Investigation of correlation between diameters of pelvic inlet and outlet planes and female pelvic floor dysfunction.

OBJECTIVE: To investigate correlation between key diameters of pelvic inlet and outlet planes and female pelvic floor dysfunction (FPFD). STUDY DESIGN: Correlation with incidence of FPFD was analyzed by measuring the two diameters of pelvic inlet and outlet planes (i.e. anteroposterior diameter of pelvic inlet and transverse diameter of pelvic outlet) in 298 patients with FPFD and 508 patients in control group taking into account of other relevant factors. RESULTS: The transverse diameter of pelvic outlet was significantly larger in experimental group than in control group (9.55cm vs. 8.50cm, P<0.01); while the difference in anteroposterior diameter of pelvic inlet between the two groups was not statistically significant (11.63cm vs. 11.26cm, P=0.205>0.01); Binary logistic regression analysis indicated that the anteroposterior diameter of pelvic inlet was not correlated with incidence of FPFD, but the transverse diameter of pelvic outlet was one of the influencing factor for FPFD. CONCLUSIONS: The transverse diameter of pelvic outlet is closely correlated with incidence of FPFD and represents one of the risk factors for FPFD; a transverse diameter of pelvic outlet greater than 9.5cm is the threshold for onset of FPFD and can be used as an early predictive index for FPFD.