Progesterone as a morphological regulatory factor of the male and female gerbil prostate.
Autor: | Fochi RA; Department of Structural and Functional Biology, Institute of Biology, State University of Campinas (UNICAMP), São Paulo, Brazil., Santos FC, Goes RM, Taboga SR |
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Jazyk: | angličtina |
Zdroj: | International journal of experimental pathology [Int J Exp Pathol] 2013 Dec; Vol. 94 (6), pp. 373-86. |
DOI: | 10.1111/iep.12050 |
Abstrakt: | Testosterone (T) and oestrogen are the main active steroid hormones in the male and female reproductive system respectively. In female rodents progesterone (P4), together with testosterone and oestrogen, has an essential role in the regulation of the oestrous cycle, which influences the prostate physiology through their oscillations. In this work we investigated how the male and female prostate gland of Mongolian gerbils responds to surgical castration at the start of puberty and what are the effects of T, oestradiol (E2) and P4 replacement, using both quantitative and qualitative methods. We also examined the location of the main steroid receptors present in the prostate. In the castrated animals of both sexes an intense glandular regression, along with disorganization of the stromal compartment, and abundant hyperplasia was observed. The replacement of P4 secured a mild recovery of the glandular morphology, inducing the growth of secretory cells and restoring the androgen receptor (AR) cells. The administration of P4 and E2 eliminated epithelial hyperplasia and intensified gland hypertrophy, favouring the emergence of prostatic intraepithelial neoplasia (PIN). In animals treated with T and P4, even though there are some inflammatory foci and other lesions, the prostate gland revealed morphology closer to that of control animals. In summary, through the administration of P4, we could demonstrate that this hormone has anabolic characteristics, promoting hyperplasia and hypertrophy, mainly in the epithelial compartment. When combined with E2 and T, there is an accentuation of glandular hypertrophy that interrupts the development of hyperplasia and ensures the presence of a less dysplastic glandular morphology. (© 2013 The Authors. International Journal of Experimental Pathology © 2013 International Journal of Experimental Pathology.) |
Databáze: | MEDLINE |
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