The effect of androgens and antiandrogens on the immunohistochemical localization of the androgen receptor in accessory reproductive organs of male rats

Paris, Frank; Weinbauer, Gerhard F.; Blüm, Volker; Nieschlag, Eberhard

doi:10.1016/0960-0760(94)90259-3

Cited by 45 publications

(21 citation statements)

References 40 publications

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“…The results of our study disagree with these findings: no changes in the rate of epithelial cells expressing AR were found in peripubertal animals with androgenic blockade. This was therefore in agreement with the studies of other authors, indicating that the treatment with antiandrogens resulted in a loss of weight of ventral prostate from adult rats but did not alter the distribution of AR-immunoreactivity (Paris et al, 1994). Moreover, the changes in expression of AR in animals with androgen blockade might be species-specific, because in other rodents, such as gerbils (M. unguiculatus), pharmacological castration decreases the AR expression (Cordeiro et al, 2008).…”

Section: Discussionsupporting

confidence: 92%

Effect of Prolactin on the Population of Epithelial Cells From Ventral Prostate of Intact and Cyproterone Acetate‐Treated Peripubertal Rats: Stereological and Immunohistochemical Study

Gómez

Ingelmo

Martı́n

et al. 2009

The Anatomical Record

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The interactions between steroid and nonsteroid hormones in the prostate are of special interest during the growth phase of the gland. The purpose of this work is to study the influence of prolactin (PL), with or without androgenic blockade, on epithelial cells from peripubertal rat ventral prostate. Twenty male peripubertal Sprague-Dawley rats were grouped as controls, or treated with cyproterone acetate (CA), CA plus PL (CA-PL), or PL. The total number (N total) of epithelial cells, and their labeling indices to proliferative cell nuclear antigen (LI PCNA), apoptosis (LI apoptosis) and androgen receptors (LI AR) were measured. CA and PL treatment significantly decrease the N total, but the LI PCNA was unchanged. We have observed a greater LI apoptosis in pharmacologically castrated animals without PL than in the rats with androgenic blockade with PL. The LI AR does not change with CA treatment in the ventral region, but the PL significantly increases it. Androgenic blockade and PL decrease the number of epithelial cells from the ventral prostate. These changes are not attributable to the decrease of cell proliferation, rather to the increase of epithelial apoptosis. The increase of cells expressing AR after treatment with PL might be attributed to the decrease of testosterone secretion caused by the hyperprolactinemia. PL does not modulate the size of the ventral prostate in prepubertal rats. Anat Rec, 292:746-755, 2009. V V C 2009 Wiley-Liss, Inc.

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Section: Discussionsupporting

confidence: 92%

Effect of Prolactin on the Population of Epithelial Cells From Ventral Prostate of Intact and Cyproterone Acetate‐Treated Peripubertal Rats: Stereological and Immunohistochemical Study

Gómez

Ingelmo

Martı́n

et al. 2009

The Anatomical Record

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“…The present study showed that nuclear AR levels in rat epididymal stromal cells are more sensitive than that in epithelial cells to circulating androgen. Similarly, compared with other tissues or organs in the male reproductive system, epididymal epithelial cells have a greater ability to maintain AR levels during androgen deprivation [32]. After treatment with an LHRH antagonist, the reduction in AR immunostaining in rat epididymal epithelial cells was not as obvious as the declines that occurred in epithelial cells of ventral prostate and seminal vesicle in one report [32].…”

Section: Discussionmentioning

confidence: 94%

Effects of Androgen on Androgen Receptor Expression in Rat Testicular and Epididymal Cells: A Quantitative Immunohistochemical Study1

Zhu

Hardy

Inigo

et al. 2000

Biology of Reproduction

119

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Androgen is essential for maintenance of spermatogenesis in the testis and for maturation of spermatozoa in the epididymis. The effects of androgen are mediated through its receptor (AR), the levels of which are, in turn, regulated by androgen. Previous studies have shown that AR concentrations in Leydig and Sertoli cells are differentially regulated during development. The aim of the present study was to determine if cell-type-specific regulation of AR by androgen occurs in testicular and epididymal cells during adulthood. Adult male rats were treated with the LHRH-antagonist Azaline B (100 g/day) by osmotic pump for 1, 2, 3, 4, or 8 wk to suppress endogenous androgen, with identical numbers of intact control animals at each time period. An androgen replacement group was simultaneously treated with the antagonist and a synthetic androgen, 7 alpha-methyl-19-nortestosterone (MENT), during the final 4 wk of the experiment. Levels of nuclear AR protein in specific cell types were quantified by immunohistochemistry in conjunction with computer-assisted image analysis. Levels of AR in testicular cells declined sharply after treatment with the LHRH antagonist. In Sertoli cells, nuclear AR levels decreased to 8% of control (P < 0. 01) after 4 wk treatment; and to 12% and 17% of control (P < 0.01) in Leydig and myoid cells, respectively. Androgen replacement resulted in complete recovery of nuclear AR levels in Sertoli cells (93%, P > 0.05) but in only partial recovery in myoid (69%, P < 0. 01) and Leydig cells (56%, P < 0.01). In the epididymis, tubular epithelial cells and stromal cells differed in their responses to the LHRH antagonist. After 1 wk, nuclear AR levels in caput stromal cells decreased dramatically to 34% of control (P < 0.01) and in cauda stromal cells to 43% (P < 0.01). In contrast, the decline of AR levels in epididymal epithelial cells was not as dramatic as that in stromal cells. After 1 wk, the decline in the caput and cauda was to 87% and 76% of control, respectively. After 8 wk, nuclear AR levels in stromal cells further declined to 1.1% in caput and 1.4% in cauda, whereas in the epithelial cells, a smaller decline in nuclear AR was noted (to 30% in the caput and 45% in the cauda). After androgen replacement with MENT, nuclear AR levels recovered to more than 90% of control in both epididymal cell types. These results indicate that AR levels in the nuclei of adult Sertoli cells depend mainly on the level of androgen, whereas in the adult Leydig and myoid cells, the androgen dependency is more limited. The results also indicate that in the epididymis, stromal cells are more sensitive than epithelial cells to the regulation of AR levels by androgen.

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“…It is important to emphasize that androgens can enter through the plasma membrane into their target cells; thus, ARs, located either in the cytoplasm or in the nucleus, bind to testosterone or 5 ␣ -dihydrotestosterone and then bind as homodimers to specific DNA elements of the promoter regions of the androgen target genes and act as transcription factors [Huhtaniemi, 2010]. Cytoplasmic AR immunolabelling has also been demonstrated by Arenas et al [2001] in newt testis as well as in rat prostate [Paris et al, 1994]. Thus, the immunoexpression of ARs in the PGCs of bullfrogs reinforces the presence of testosterone in these cells, as previously demonstrated [Sasso-Cerri et al, 2005], and indicates that this steroid binds to these receptors and plays a role in these cells.…”

Section: Discussionmentioning

confidence: 99%

Primordial Germ Cells (Spermatogonial Stem Cells) of Bullfrogs Express Sex Hormone-Binding Globulin and Steroid Receptors during Seasonal Spermatogenesis

Caneguim

Beltrame

Luz

et al. 2012

Cells Tissues Organs

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In vertebrate species, testosterone seems to inhibit spermatogonial differentiation and proliferation. However, this androgen can also be converted, via aromatase, into estrogen which stimulates spermatogonial differentiation and mitotic activity. During seasonal spermatogenesis of adult bullfrogs Lithobates catesbeianus, primordial germ cells (PGCs) show enhanced testosterone cytoplasm immunoexpression in winter; however, in summer, weak or no testosterone immunolabelling was observed. The aim of this study was to confirm if PGCs express stem cell markers – alkaline phosphatase (AP) activity and GFRα1 (glial-cell-line-derived neurotrophic factor) – and verify whether testosterone is maintained in these cells by androgen receptors (ARs) and/or sex hormone-binding globulin (SHBG) in winter. Furthermore, regarding the possibility that testosterone is converted into estrogen by PGCs in summer, the immunoexpression of estrogen receptor (ER)β was investigated. Bullfrog testes were collected in winter and in summer and were embedded in glycol methacrylate for morphological analyses or in paraffin for the histochemical detection of AP activity. GFRα1, AR, SHBG and ERβ expression were detected by Western blot and immunohistochemical analyses. The expression of AP activity and GFRα1 in the PGCs suggest that these cells are spermatogonial stem cells. In winter, the cytoplasmic immunoexpression of ARs and SHBG in the PGCs indicates that testosterone is maintained by these proteins in these cells. The cytoplasmic immunoexpression of ERβ, in summer, also points to an ER-mediated action of estrogen in PGCs. The results indicate a participation of testosterone and estrogen in the control of the primordial spermatogonia during the seasonal spermatogenesis of L. catesbeianus.

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The effect of androgens and antiandrogens on the immunohistochemical localization of the androgen receptor in accessory reproductive organs of male rats

Cited by 45 publications

References 40 publications

Effect of Prolactin on the Population of Epithelial Cells From Ventral Prostate of Intact and Cyproterone Acetate‐Treated Peripubertal Rats: Stereological and Immunohistochemical Study

Effect of Prolactin on the Population of Epithelial Cells From Ventral Prostate of Intact and Cyproterone Acetate‐Treated Peripubertal Rats: Stereological and Immunohistochemical Study

Effects of Androgen on Androgen Receptor Expression in Rat Testicular and Epididymal Cells: A Quantitative Immunohistochemical Study1

Primordial Germ Cells (Spermatogonial Stem Cells) of Bullfrogs Express Sex Hormone-Binding Globulin and Steroid Receptors during Seasonal Spermatogenesis

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