The results suggest that bladder injection of MSCs ameliorates inflammation and fibrosis in bladder tissues, bladder overactivity, and nociception in a rat model of chemically induced cystitis.

Objectives To examine the correlation among bladder inflammation, angiogenesis, fibrosis and urothelial denudation in biopsied bladder specimens, and O'Leary‐Sant symptom indexes, O'Leary‐Sant problem indexes and visual analog scale pain scores in interstitial cystitis/bladder pain syndrome patients with or without Hunner lesions (Hunner type interstitial cystitis or non‐Hunner type interstitial cystitis). Methods Bladder biopsied tissues were collected from 12 Hunner type interstitial cystitis female patients, 12 non‐Hunner type interstitial cystitis female patients and 12 age‐matched non‐interstitial cystitis female patients (controls). Immunohistochemical stainings of tissue necrotic factor‐α, mast cell tryptase, vascular endothelial growth factor, CD31, transforming growth factor‐β, SLUG associated with epithelial mesenchymal transition and E‐cadherin as well as Masson trichrome staining were evaluated. The significant correlation between the expression of tissue necrotic factor‐α, mast cell tryptase, vascular endothelial growth factor, CD31, transforming growth factor‐β, collagen, SLUG or E‐cadherin, and O'Leary‐Sant symptom indexes, O'Leary‐Sant problem indexes or visual analog scale pain scores was then examined. Results The expression of tissue necrotic factor‐α, vascular endothelial growth factor, CD31, transforming growth factor‐β and SLUG was significantly increased in non‐Hunner type interstitial cystitis and Hunner type interstitial cystitis patients compared with controls whereas the significant increases in the expression of mast cell tryptase and collagen were observed in Hunner type interstitial cystitis patients compared with controls and non‐Hunner type interstitial cystitis patients. On the other hand, the expression of E‐cadherin was significantly decreased in Hunner type interstitial cystitis patients compared with controls and non‐Hunner type interstitial cystitis patients. In addition, the increased expression of CD31 in bladder tissues was strongly correlated with O'Leary‐Sant symptom indexes, O'Leary‐Sant problem indexes and visual analog scale pain scores. Conclusions These results suggest that bladder angiogenesis evident as the increased expression of CD31 is strongly correlated with urinary frequency and bladder pain in patients with non‐Hunner type interstitial cystitis and Hunner type interstitial cystitis.

Benign Prostatic Hyperplasia (BPH) is an age-related debilitating prostatic disease that is frequently associated with prostatic inflammation and bothersome lower urinary tract symptoms (LUTS). Animal models have shown that formalin- and bacterial-induced prostatic inflammation can induce bladder dysfunction; however, the underlying mechanisms contributing to prostatic inflammation in BPH and bladder dysfunction are not clear. We previously reported that E-cadherin expression in BPH is down-regulated in hyperplastic nodules compared to expression in adjacent normal tissues. Here, we explored the potential consequences of prostatic E-cadherin down-regulation on the prostate and bladder in vivo using an inducible murine model of prostate luminal epithelial-specific deletion of Cdh1. The PSA-CreER T2 transgenic mouse strain expressing tamoxifen-inducible CreER T2 recombinase driven by a 6-kb human PSA promoter/enhancer was crossed with the B6.129-Cdh1  tm2Kem/J mouse to generate bigenic PSA-CreER T2/Cdh1  -/- mice. Deletion of E-cadherin was induced by transient administration of tamoxifen when mice reached sexual maturity (7 weeks of age). At 21-23 weeks of age, the prostate, bladder, and prostatic urethra were examined histologically, and bladder function was assessed using Void Spot Assays and cystometry. Mice with Cdh1 deletion had increased prostatic inflammation, prostatic epithelial hyperplasia and stromal changes at 21-23 weeks of age, as well as changes in bladder voiding function compared to age-matched controls. Thus, loss of E-cadherin in the murine prostate could result in prostatic defects that are characteristic of BPH and lower urinary tract symptoms, suggesting that E-cadherin down-regulation could be a driving force in human BPH development and progression.

Purpose: To investigate the influence of multiple recurrences and repeated surgeries of Hunner lesions on bladder capacity under general anesthesia in patients with interstitial cystitis (IC).Methods: We retrospectively reviewed the clinical records of Hunner-type IC (HIC) patients who underwent transurethral fulguration or resection of Hunner lesions combined with hydrodistension by a single surgeon between 2011 and 2020. Recurrence was defined as reappearance of uncontrolled urinary symptoms in association with new Hunner lesions identified by cystoscopy. Recurrent Hunner lesions were then treated by transurethral surgeries. The recurrence-free rate, potential predictive factors of recurrence, and changes in bladder capacity under anesthesia were examined at each surgical procedure.Results: A total of 92 surgeries were performed in 47 HIC patients, 23 (49%) of whom required multiple procedures (range, 1–5 times). The mean recurrence-free time after the first surgery was 21.7 months. The recurrence-free rate was 53% at 24 months, and decreased to 32% at 48 months. There were no significant differences in age, sex, bladder capacity under anesthesia at the first surgery, duration from symptom onset to the first surgery, O’Leary-Sant questionnaire including symptom and problem indexes, visual analogue scale pain score, and the number of comorbidities between the cases with or without recurrence. Bladder capacity under anesthesia was gradually decreased as the number of surgeries was increased, and bladder capacity at the fourth procedure was significantly decreased to 80% of the capacity at the first surgery.Conclusions: These results suggest that multiple recurrences and repeated surgeries of Hunner lesions result in a reduction of bladder capacity under anesthesia in HIC patients although no predictive factors for recurrence of Hunner lesions were detected.

These results suggest that the combination therapy of tadalafil and tamsulosin can induce the additive inhibitory effects on urinary frequency compared with monotherapy, more likely via inhibition of the afferent limb of micturition reflex rather than the efferent function as evidenced by the increases in threshold pressures and intercontraction intervals without affecting bladder contractile function.