Project description:Pelvic organ prolapse (POP) is a common pelvic floor disorder characterized by the descent of pelvic organs and progressive remodeling of pelvic floor support tissues. To investigate the molecular changes associated with POP, we established a mouse model by combining bilateral ovariectomy, cervical traction, and repeated vaginal distension in female C57BL/6 mice. Vaginal tissues were collected from mice in the POP and control groups for transcriptomic analysis. Bulk RNA sequencing was performed on three biological replicates from the POP group and three biological replicates from the control group. This dataset provides transcriptomic profiles of vaginal tissues associated with experimentally induced POP and may facilitate the identification of molecular pathways involved in pelvic floor tissue remodeling during POP development.
Project description:Long-term menopause is considered to be one of the risk factors for pelvic organ prolapse. In the case of long-term menopause, the supporting function of the pelvic floor tissue is weakened, but the effect on the vaginal wall tissue is not fully elaborated. This study intends to use transcriptomics to further clarify.
Project description:Fecal incontinence is common in patients with rectal cancer after surgery. Previous studies showed that pelvic floor muscle and external sphincter muscle training after stoma closure could improve the severity of incontinence and other fecal symptoms, but there is no study about the effects of pelvic floor muscle exercise intervention before stoma closure. We are wondering would the symptom of fecal incontinence recover sooner and better if we give the pelvic floor muscle exercise intervention before the stoma closure. This article aims at comparing the effects of pelvic floor muscle training before stoma closure on fecal incontinence (pre-intervention group) with pelvic floor muscle training after stoma closure (post-intervention group), and we hypothesise that the severity of fecal incontinence will improve sooner and better in pre-intervention group.
Project description:Purpose: This study aimed to investigate the imaging characteristics and molecular mechanisms by which pelvic floor electrical stimulation (PFES) improves pelvic floor muscle injury in a rat model of stress urinary incontinence (SUI). Methods: An SUI model was established in female Sprague-Dawley rats via vaginal distension combined with bilateral ovariectomy. One week post-modeling, the stimulation group received intravaginal PFES for 2 weeks. Evaluations included 9.4 T MRI, urodynamic tests, histopathological staining, qPCR, Western blotting, and RNA-seq. Results: PFES significantly elevated ALPP compared with controls, indicating improved urinary continence. MRI demonstrated that PFES attenuated focal hyperintensity, muscle edema, and fiber disorganization in the pubococcygeus muscle. Histological analyses confirmed that PFES restored dense muscle fiber arrangement and collagen distribution, and immunohistochemistry showed upregulated expression of COL1A1, COL3A1, and CD34. RNA-seq revealed that differentially expressed genes were prominently enriched in ECM organization, focal adhesion, ECM-receptor interaction, and the PI3K-Akt pathway. Western blotting verified that PFES increased COL1A1, COL3A1, and VEGFA, while suppressing the atrophy-related ubiquitin ligase FBXO32. Conclusion: PFES effectively repairs pelvic floor muscle structure and function by reducing muscle edema and fiber disruption, upregulating type I and III collagens to promote ECM remodeling, inducing VEGF-mediated angiogenesis, and downregulating FBXO32 to counteract atrophy. These findings elucidate PFES mechanisms and support its clinical application.
2026-08-13 | GSE343122 | GEO
Project description:Imaging and Molecular Mechanisms of Pelvic Floor Electrical Stimulation in Improving Pelvic Floor Muscle Injury in Stress Urinary Incontinence Rats
Project description:Healthy pelvic floor muscles (PFMs) are essential for proper pelvic floor function. The biggest risk factor for PFM dysfunction is injury sustained during vaginal childbirth, yet the factors that facilitate or impair PFM recovery from birth injury remain unknown. We aimed to assess the impact of the postpartum milieu in the presence and absence of lactation on PFM regeneration following simulated birth injury (SBI) in a pregnant rat model. We determined that lactating rats have a rapid increase in systemic immune markers in response to SBI, which contributes to rapid changes in PFM immune cell infiltration and decrease in pro-inflammatory genes. PFMs in lactating rats have enrichment of anti-inflammatory genes and larger newly formed myofibers that contribute to larger myofiber size after weaning. This suggests that lactation promotes an earlier anti-inflammatory response in injured PFMs that allows for quicker myogenesis and myofiber hypertrophy.
Project description:<p>The overall purpose of this University of Utah Pelvic Organ Prolapse Disorder Study was to identify and localize predisposition genes contributing to pelvic organ prolapse (POP). POP cases recruited for this study were identified by one of three methods: high-risk POP pedigree cases, POP sister pairs, and surgically-treated POP cases reporting a family history of POP. <b>High-risk POP pedigree cases</b> were identified using the Utah Population Database (UPDB), a genealogy database of residents in Utah that has been linked to diagnostic ICD9 and CPT codes in medical records at the University of Utah and Intermountain Healthcare. We identified families with a significant excess number of POP cases compared to matched population rates and targeted these individuals for recruitment as well as any other POP cases in the family. <b>POP sister pair cases</b> were identified at the University of Utah Urogyncology clinic for women who had undergone POP surgery and also self-reported one or more sisters who were also surgically treated for POP. POP affection status of all sisters was confirmed either by physical examination or by chart review. <b>Surgically treated-POP cases reporting a family history of POP</b> were identified at the University of Utah Urogyncology clinic by self-report of a family history of POP. Efforts were made to recruit other affected family members and confirm affection status. To obtain DNA, subjects provided either a blood specimen or saliva. Medical records were reviewed by a urogynecologist and diagnostic information for pelvic organ prolapse and stress and overactive bladder were obtained. Collected DNA was genotyped and analyzed. To maintain confidentiality of the familial data, genetic data from only one subject per family has been submitted to dbGaP.</p> <p>Use of the University of Utah Pelvic Organ Prolapse Disorder Study data is limited to investigators studying pelvic floor disorders. These pelvic floor disorders include pelvic organ prolapse, urinary and anal incontinence, and other conditions related to weakening or injury to the muscles and connective tissue in the pelvis as a result of pelvic surgery, pregnancy, or vaginal delivery of a child. These data will be used only for research purposes related to pelvic floor disorders. They will not be used to determine the individual identity of any person or their relationship to another person or for research on non-disease traits.</p>