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Ultrastructural changes in prostate cells during hormone-induced canine prostatic hyperplasia
Fanny Gallardo-Arrieta1, Teresa Mogas, Luís Magán
1Departament de Medicina i Cirurgia Animals, Facultat de Veterinaria, Autonomous University of Barcelona, Barcelona, Spain.
Ultrastructural Pathology
|December 22, 2006
Summary
Canine prostatic hyperplasia, a condition affecting dogs and humans, was studied using an experimental model. Researchers observed unique ultrastructural changes in basal cells, suggesting new avenues for understanding this common disease.
Area of Science:
- Veterinary Pathology
- Cell Biology
- Urology
Background:
- Benign prostatic hyperplasia (BPH) is a common condition with significant morbidity and social impact.
- Few animal models exist for studying BPH, limiting research.
- Dogs spontaneously develop BPH with age, similar to humans, making them a valuable model.
Purpose of the Study:
- To compare ultrastructural changes in experimentally induced canine BPH with spontaneous changes in untreated dogs.
- To investigate the utility of an experimental canine BPH model for further research.
Main Methods:
- An experimental group of 5 male beagle dogs were castrated and treated with combined steroids for over 30 weeks.
- Prostate samples were collected at regular intervals.
- A control group of 3 noncastrated dogs received vehicle treatment, with samples collected at specific stages.
Main Results:
- Both experimental and control groups showed BPH changes, with more intensity in the experimental group.
- Luminal cells exhibited papillary projections, prominent microvilli, and abundant granules.
- A novel finding was the presence of caveolae in basal cells, particularly prominent in the experimental group and advanced stages.
Conclusions:
- The experimentally induced canine BPH model adequately replicates spontaneous changes.
- The newly identified ultrastructural changes in basal cells warrant further investigation in both canine and human BPH.
- This model provides a suitable platform for understanding the mechanisms of benign prostatic hyperplasia.

