Abstract
Non-invasive biomarkers to identify patients with bladder outlet obstruction (BOO)-related dysfunction are still needed to guide clinical practice. The current study aims to investigate molecular alterations and biomarkers associated with partial BOO (PBOO) in rats. Sprague–Dawley rats were used to establish the BOO model. Serum samples from 60 patients with benign prostatic hyperplasia (BPH) were used for enzyme-linked immunosorbent assay analysis. RNA sequencing and TMT-labeling proteomic analyses were conducted to identify molecular alterations. Masson’s trichrome, H&E, and immunohistochemical staining and western blotting were conducted by using conventional methods following the manufacturer’s instructions. Rats with PBOO experienced hypertrophy of smooth muscle cells and hyperplasia of interstitial cells during the first 4 weeks after the initiation of obstruction. Four weeks later, rats with PBOO showed activation of the adaptive immune response, cell death and apoptosis. The levels of brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF2) in the serum gradually increased in the first 4 weeks and gradually decreased after week 4. FGF2 levels slightly correlated with prostate volume (R = 0.156, P = 0.0028) but not with age or BMI in BPH patients. No correlations were found between BDNF levels and prostate volume, age or BMI. BOO induces a change from bladder compensation to decompensation at week 4. FGF2 is involved in the development of hypertrophy in the PBOO bladder and shows a positive correlation with prostate volume in BPH patients.
Highlights
Bladder outlet obstruction (BOO), defined as a high-pressure/low-flow micturition pattern on urodynamic investigation, is a consequence of benign prostatic hyperplasia (BPH) in aging men, bladder neck obstruction (BNO), posterior urethral valve (PUV), and urethral stricture (US) (Metcalfe et al, 2010)
Identifying the function of bladder depend on urodynamics examination, bladder wall thickness (BWT), detrusor wall thickness (DWT) with imaging test, questionnaire of International Prostate Symptom Score (IPSS), et al no international standards or guidelines were made to standardize the diagnosis and we still lack non-invasive techniques or biomarkers to identify which patients are at increased risk of bladder outlet obstruction (BOO)-related bladder dysfunction
We found that the level of brain-derived neurotrophic factor (BDNF) was higher in rats with partial BOO (PBOO) at week 4 and gradually decreased after week 5
Summary
Bladder outlet obstruction (BOO), defined as a high-pressure/low-flow micturition pattern on urodynamic investigation, is a consequence of benign prostatic hyperplasia (BPH) in aging men, bladder neck obstruction (BNO), posterior urethral valve (PUV), and urethral stricture (US) (Metcalfe et al, 2010). An estimated 917 million individuals worldwide experienced lower urinary tract symptoms (LUTS)/BOO in 2008, with the number of affected individuals projected to increase by 9.3% to 1.0 billion in 2013 and by 18.5% to 1.1 billion in 2018 (Irwin et al, 2011). The prevalence of this condition in women has been estimated to be between 2.7 and 29%, and women report fewer classic obstructive symptoms than men (Patel and Nitti, 2001). Non-invasive markers offer some advantages such as reduced risk of sampling error, objectiveness in the interpretation of the result, appropriateness for repeated measurements and lower cost
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