It has been shown that TGF-β mediates EMT in BPH via activation of Smad signaling 12. BPH has been associated with decreased E-cadherin expression and accumulation of mesenchymal-like cells derived from the prostatic epithelium and the endothelium, changes consistent with epithelial-to-mesenchymal transition (EMT) 10, 11, 12. Notably, there is a reduction in neuroendocrine cells and a particular fibroblast cell type that expresses estrogen receptors near the epithelium, while there is an increase in a subset of myofibroblasts 6. Instead, there is a distinct depletion and enrichment of specific prostate cell types found in both the BPH epithelium and stroma. According to recent genomic analyses of BPH, it has been discovered that this condition is not simply characterized by prostatic hyperplasia. Additionally, heightened inflammation associated with metabolic syndrome has been identified as a factor that can impact the prostatic stroma and is considered a determining factor in prostate enlargement 9. As individuals age, these stromal signals can be reactivated, contributing to the pathogenesis of BPH 6, 8. In the normal development of the prostate gland, androgens primarily influence the stroma, which then regulates the proliferation and differentiation of prostatic epithelial cells 6, 7. ![]() The pathophysiology of BPH has been associated with androgen signaling, reactive stroma and inflammation 5, 6. In addition to these symptoms, serious complications frequently occur such as renal failure, bladder stones, urinary bleeding and infections. Symptoms include increased urinary frequency and urgency to acute urinary retention. The prevalence of BPH is widespread, with the disease incidence increasing by 10% every decade and approximately 50% of men aged 50 years are diagnosed with histologic BPH 4. As a result, men experience lower urinary tract symptoms (LUTS) caused by obstruction of the bladder outlet 1, 2, 3. This enlargement occurs due to excessive growth of the epithelial and stromal cells within the prostate. Considering the large incidences of BPH and its associated economic burdens, our study has important implications and can potentially improve the clinical management of BPH.īenign prostatic hyperplasia (BPH) is a condition characterized by the gradual enlargement of the prostate gland's transition zone. Furthermore, these vesicles attenuated bone morphogenic protein 5 (BMP5) signaling, a cardinal alteration that is instrumental in driving BPH. Remarkably, POM-NVs could reverse the BPH phenotype conferred by TGF-β mediated signaling and induced epithelial-to-mesenchymal (EMT) reversal, leading to the restoration of prostate epithelial states in vivo and in vitro. We further tested these vesicles using a clinically relevant xenograft mouse BPH model derived from human BPH tissues. Following extensive characterization of POM-NVs, we tested their therapeutic potential in vitro using BPH1 cell line and identified a potential anti-proliferative and pro-apoptotic effect. We isolated nanovesicles from pomegranate juice ( Punica Granatum) (referred to as ‘POM-NVs’) and report to our knowledge for the first time, that these vesicles possess therapeutic potential against BPH. ![]() ![]() Current therapies include 5-alpha reductase inhibitors and alpha-blockers that are only partially effective and pose a huge economic burden, emphasizing the urgent need for effective, economical therapies. ![]() Benign prostatic hyperplasia (BPH) and associated lower urinary tract symptoms affect a large percentage of the male population and places a substantial burden on the world health system.
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