In ageing men, benign prostatic hyperplasia (BPH) is a chronic disease that leads to progressive lower urinary tract symptoms (LUTS) caused by obstruction of the bladder outlet (BOO). Patients with LUTS (such as increased frequency and urgency of urination) and complications of BOO (such as hydronephrosis and bladder stones) are at risk of serious health problems. BPH causes a rapidly rising burden of LUTS far exceeding that of other urological conditions. Treatment outcomes are unsatisfactory for BPH largely due to the lacking of fully understanding of the pathogenesis. Hormonal imbalances related to androgen and oestrogen can cause BPH, but the exact mechanism is still unknown, even the animal model is not fully understood. Additionally, there are no large-scale data to explain this mechanism. A BPH mouse model was established using mixed slow-release pellets of testosterone (T) and estradiol (E2), and we measured gene expression in mouse prostate tissue using RNA-seq, verified the results using qRT‒PCR, and used bioinformatics methods to analyse the differentially expressed genes (DEGs).

In aging men, BPH is a chronic disease that leads to progressive lower urinary tract symptoms (LUTS) caused by obstruction of the bladder outlet (BOO). Patients with LUTS (such as frequency and urgency) and complications of BOO (such as hydronephrosis and bladder stones) are at risk of serious health problems. Nevertheless, clinical treatment is complicated and uncertain. BPH is caused by hormonal imbalances related to androgen and estrogen, but the exact mechanism is still unknown, even the animal model is not fully understood. However, there are no large-scale data to explain this mechanism. A BPH mouse model was established using mixed slow-release pellets of testosterone (T) and estradiol (E2), and we detected gene expression in mouse prostate tissue using RNA-seq, and verified the results using qRT-PCR, and used bioinformatics methods to analyze the differentially expressed genes (DEGs).