Hormonal therapy in the senescence: Prostatic microenvironment structure and adhesion molecules
Fábio Montico1, Amanda Cia Hetzl, Eduardo Marcelo Cândido
1Department of Anatomy, Cell Biology, Physiology and Biophysics, Institute of Biology, State University of Campinas (UNICAMP), 13083-865 Campinas, São Paulo, Brazil. fabio260287@gmail.com
Micron (Oxford, England : 1993)
|April 15, 2011
Summary
Hormone replacement therapy in aging rats showed mixed results for prostate health. While it improved dystroglycan levels, it also worsened age-related structural changes, suggesting potential hormonal imbalance.
Area of Science:
- Endocrinology
- Urology
- Cell Biology
Background:
- Hormonal imbalance is common in elderly men, potentially affecting prostate health.
- The precise impact of hormone replacement therapy (HRT) on prostatic diseases in aging is not fully understood.
Purpose of the Study:
- To investigate the structural and molecular changes in the ventral prostate of elderly rats undergoing steroid hormone replacement.
- To analyze the reactivity of dystroglycan (DG) molecules in response to HRT in senescent prostates.
Main Methods:
- Elderly rats were subjected to various treatments: senescence, testosterone, estrogen, castration, and combined castration-hormone therapies.
- Ventral prostate tissues were analyzed using light and transmission electron microscopy, morphometry, immunohistochemistry, and Western Blotting.
- Serum hormone levels were measured to confirm treatment efficacy.
Main Results:
- Hormone administration effectively altered serum testosterone and estrogen levels.
- Senescent and HRT-treated groups exhibited atrophic epithelium, stromal hypertrophy, and inflammatory cells.
- Dystroglycan (DG) levels decreased in senescence but increased with HRT, particularly with estrogen therapy.
Conclusions:
- Hormonal therapy in senescent rats shows positive effects on dystroglycan levels, crucial for epithelial-stromal interactions.
- However, HRT may exacerbate senescence-associated prostatic structural changes, possibly due to androgen-estrogen imbalance.
- The findings suggest a complex stromal microenvironment response to HRT, potentially influencing glandular lesion development.
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