Translational andrology and urology · 2025
Immunohistochemical study of Rho-kinase pathway expression in a mouse model of prostate hypertrophy for preliminary study of progressive prostate cancer model establishment.
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Yang Young-Min, Kitagawa Koichi, Hirata Yuto, Moriwaki Michika, Ono Tenei, Chiang Yi-Te, Chen Kuan-Chou, Shigemura Katsumi
Аннотация
BACKGROUND: For aggressive prostate research, a suitable orthotopic animal model is in demand. This study aims to future establishment of mice prostate cancer model via testosterone dosing after castration, and, as a preliminary experiment, evaluate the changes in prostate and bladder caused by benign prostate hyperplasia (BPH). An animal prostate enlargement model was used to assess bladder smooth muscle changes via immunohistochemical (IHC) markers of the prostate and bladder.
METHODS: Injection of testosterone propionate into 12-week-old C57BL/6 mice stimulated prostatic hypertrophy in a mouse model. Three groups of mice were divided into control, castrated mice with a single subcutaneous dose of 50 μL testosterone administration, castrated mice without testosterone administration, and sacrificed 4 weeks later. α-1 adrenoceptor and transforming growth factor-beta (TGF-β) expression in the prostate ventral lobe and β-3 adrenoceptor and Rho-kinase expression in the bladder mucosa were evaluated by IHC staining analyses and compared among the 3 groups.
RESULTS: Prostate weights for the control, castrated, and castrated + testosterone groups were 75±27, 101.9±17, and 130±19 mg, respectively, showing a significant difference in prostate weight between the subject and castration plus treatment groups (P<0.05). IHC data showed that the castrated + testosterone group had significantly higher expression of α-1 adrenoceptor antibody (0±0 vs. 1.25±0.433, P=0.02) in the prostate ventral lobe and β-3 adrenoceptor antibody (0±0 vs. 1±1.41, P=0.0003) and Rho-kinase antibody (0±0 vs. 2±0, P=0.0001) in the bladder mucosa, compared with the control groups.
CONCLUSIONS: For our establishment of a prostate cancer model for mice, our in vivo experiments using IHC study demonstrated that the overexpression of α-1 adrenoceptor (prostate enlargement), β-3 adrenoceptor and Rho-kinase (bladder) biomarkers indicated that prostate enlargement can cause bladder muscle atrophy. Further research could be undertaken using this prostate enlargement model for cancer research.
METHODS: Injection of testosterone propionate into 12-week-old C57BL/6 mice stimulated prostatic hypertrophy in a mouse model. Three groups of mice were divided into control, castrated mice with a single subcutaneous dose of 50 μL testosterone administration, castrated mice without testosterone administration, and sacrificed 4 weeks later. α-1 adrenoceptor and transforming growth factor-beta (TGF-β) expression in the prostate ventral lobe and β-3 adrenoceptor and Rho-kinase expression in the bladder mucosa were evaluated by IHC staining analyses and compared among the 3 groups.
RESULTS: Prostate weights for the control, castrated, and castrated + testosterone groups were 75±27, 101.9±17, and 130±19 mg, respectively, showing a significant difference in prostate weight between the subject and castration plus treatment groups (P<0.05). IHC data showed that the castrated + testosterone group had significantly higher expression of α-1 adrenoceptor antibody (0±0 vs. 1.25±0.433, P=0.02) in the prostate ventral lobe and β-3 adrenoceptor antibody (0±0 vs. 1±1.41, P=0.0003) and Rho-kinase antibody (0±0 vs. 2±0, P=0.0001) in the bladder mucosa, compared with the control groups.
CONCLUSIONS: For our establishment of a prostate cancer model for mice, our in vivo experiments using IHC study demonstrated that the overexpression of α-1 adrenoceptor (prostate enlargement), β-3 adrenoceptor and Rho-kinase (bladder) biomarkers indicated that prostate enlargement can cause bladder muscle atrophy. Further research could be undertaken using this prostate enlargement model for cancer research.