Evidence map›Paper›PMID 41522316›Full record

ArticleTranslational andrology and urology2025

Immunohistochemical study of Rho-kinase pathway expression in a mouse model of prostate hypertrophy for preliminary study of progressive prostate cancer model establishment.

Young-Min Yang, Koichi Kitagawa, Yuto Hirata, Michika Moriwaki, Tenei Ono, Yi-Te Chiang, Kuan-Chou Chen, Katsumi Shigemura

Abstract read
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Article in Translational andrology and urology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Young-Min YangDepartment of Urology, Kobe University Graduate School of Medicine, Kobe, Japan.
Koichi KitagawaDepartment of Advanced Medical Science, Graduate School of Science, Technology and Innovation, Kobe University, Kobe, Japan.
Yuto HirataDepartment of International Health, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Michika MoriwakiDepartment of International Health, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Tenei OnoDepartment of Urology, Teikyo University Hospital, Tokyo, Japan.
Yi-Te ChiangDepartment of Urology, Shuang Ho Hospital, Taipei Medical University, New Taipei City.
Kuan-Chou ChenDepartment of Urology, Shuang Ho Hospital, Taipei Medical University, New Taipei City.
Katsumi ShigemuraDepartment of Urology, Teikyo University Hospital, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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 Conclusions: For our establishment of a prostate cancer model for mice, our

Indexed as

animal studybladder muscle atrophyProgressive prostate cancer model establishmentprostatic hyperplasia

Identifiers

PMID41522316
PMCPMC12779437

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.