ArticleLaboratory investigation; a journal of technical methods and pathology2015
Increased susceptibility of estrogen-induced bladder outlet obstruction in a novel mouse model.
Article in Laboratory investigation; a journal of technical methods and pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- A scoping review of the role of heritability and environmental exposures in the development and severity of benign prostatic hyperplasia.Translational andrology and urology · 2025Review
- Bisphenol A Effects on Neurons' Neurochemical Character in the Urinary Bladder Intramural Ganglia of Domestic Pigs.International journal of molecular sciences · 2023Article
- Bisphenol-A analogs induce lower urinary tract dysfunction in male mice.Biochemical pharmacology · 2022Article
- Male Lower Urinary Tract Dysfunction: An Underrepresented Endpoint in Toxicology Research.Toxics · 2022Review
- Bisphenol A affects vipergic nervous structures in the porcine urinary bladder trigone.Scientific reports · 2021Article
- [Outcome of surgical management and pathogenesis of female primary bladder neck obstruction].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2019Article
- High butter-fat diet and bisphenol A additively impair male rat spermatogenesis.Reproductive toxicology (Elmsford, N.Y.) · 2017Article
- In Utero and Lactational TCDD Exposure Increases Susceptibility to Lower Urinary Tract Dysfunction in Adulthood.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Disorders of the prostate and lower urinary tract are common in elderly men. We investigated the role of metallothionein-1 (MT1) in prostate carcinogenesis by generating a prostate-specific, MT1-expressing mouse. Unexpectedly, genomic analyses revealed that a 12.1-kb genomic region harboring several conserved noncoding elements was unintentionally deleted, upstream of the transgene integration site in the mouse, which we named it 12.1ΔMT1. Male 12.1ΔMT1 mice chronically treated with testosterone (T) plus 17β-estradiol (E2) to induce prostate cancer exhibited no evidence of precancerous or cancerous lesions. Instead, most of them exhibited a bladder outlet obstruction (BOO) phenotype not observed in treated wild-type (WT) mice. Thus, we hypothesized that 12.1ΔMT1 is a novel model for studying the hormonal requirement for BOO induction. Adult male 12.1ΔMT1 and WT mice were treated with T, E2, bisphenol A (BPA), T+E2, or T+BPA for up to 6 months. Histologic and immunohistochemical analysis of the prostate, bladder, and urethra were performed. No significant prostate pathologies were observed in WT or 12.1ΔMT1 mice treated with any of the hormone regimens. As expected, prostatic regression occurred in all E2-treated animals (WT and 12.1ΔMT1). Of great interest, despite a small prostate, 100% of E2-treated 12.1ΔMT1 mice, but only 40% of E2-treated WT mice, developed severe BOO (P<0.01). In contrast, T+E2 treatment was less effective than E2 treatment in inducing severe BOO in 12.1ΔMT1 mice (68%, P<0.05) and was completely ineffective in WT animals. Similarly, T, BPA, and T+BPA treatments did not induce BOO in either WT or 12.1ΔMT1 mice. The BOO pathology includes a thinner detrusor wall, narrowing of bladder neck and urethral lumen, and basal cell hyperplasia in the bladder body and urethra. These findings indicate that 12.1ΔMT1 mice exhibit enhanced susceptibility to E2-induced BOO that is independent of prostate enlargement but that is attenuated by the conjoint treatment with T.
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