Effect of hyperprolactinemia on PRL-receptor expression and activation of Stat and Mapk cell signaling in the prostate of long-term sexually-active rats

Pascual-Mathey, L.I.; Rojas-Durán, Fausto; Aranda-Abreu, Gonzálo Emiliano; Manzo, Jorge; Herrera-Covarrubias, Deissy; Muñoz-Zavaleta, David A.; Hernández, Luis García; Hernández-Aguilar, María Elena

doi:10.1016/j.physbeh.2016.02.011

Cited by 13 publications

(14 citation statements)

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“…In our experiment, castrated rats treated with prolactin for 3 or 10 days also demonstrated an increase of STAT3 expression. STAT5 also showed a tendency to be upregulated in both PRL groups, but without statistical difference, as observed by Pasqual-Mathey and coworkers (Pascual-Mathey et al 2016). Overall, these results reinforce the important role of STAT3 in the response to prolactin in the rat VP.…”

Section: Discussionsupporting

confidence: 85%

“…It has been demonstrated that active sexual life produces a constant increase in serum prolactin levels, which is associated with the production of quantity and quality of prostatic semen to ensure fertilization (Rojas-Durán et al 2015;Pascual-Mathey et al 2016). In an experimental model of hyperprolactinemia induced by intraperitoneal prolactin injection or adenohypophysis transplantation under the renal capsule, Pascual-Mathey and coworkers demonstrated a sustained activation of the signaling pathway downstream to prolactin, involving its receptors, p-Stat3, and the MAPK pathway in VP of non-castrated rats, associating these results to the increase of synthesis and secretion of the prostatic fluid (Pascual-Mathey et al 2016). In our experiment, castrated rats treated with prolactin for 3 or 10 days also demonstrated an increase of STAT3 expression.…”

Section: Discussionmentioning

confidence: 99%

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The prostate response to prolactin modulation in adult castrated rats subjected to testosterone replacement

et al. 2017

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Despite the androgenic dependence, other hormones, growth factors, and cytokines are necessary to support prostatic growth and maintain the glandular structure; among them, prolactin is a non-steroidal hormone secreted mainly by the pituitary gland. However, extra-pituitary expression of prolactin, such as in the prostate, has also been demonstrated, highlighting the paracrine and autocrine actions of prolactin within the prostate. Here, we investigated whether prolactin modulation alters ventral prostate (VP) morphophysiology in adult castrated rats. Sprague Dawley rats were castrated and after 21 days, divided into ten experimental groups (n = 6/group): castrated control: castrated animals that did not receive treatment; castrated+testosterone: castrated animals that received T (4 mg/kg/day); castrated+PRL (PRL): castrated animals receiving prolactin (0.3 mg/kg/day); castrated+T+PRL: castrated animals that received a combination of testosterone and prolactin; and castrated+bromocriptine (BR): castrated animals that received bromocriptine (0.4 mg/kg/day). The control group included intact animals. The animals were treated for 3 or 10 consecutive days. At the end of experimental period, the animals were euthanized, and the blood and VP lobes were collected and analyzed by different methods. The main findings were that the administration of prolactin to castrated rats did not exert anabolic effects on the VP. Although we observed activation of downstream prolactin signaling after prolactin administration, this was not enough to overcome the prostatic androgen deficiency. Likewise, there was no additional glandular involution in the castrated group treated with bromocriptine. We concluded that despite stimulating the downstream signaling pathway, exogenous prolactin does not act on VP in the absence or presence of high levels of testosterone.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

The prostate response to prolactin modulation in adult castrated rats subjected to testosterone replacement

et al. 2017

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“…The short isoforms also exhibit long isoform-independent activities upon PRL engagement [16]. Thus, the activated pathway and the resulting PRL effector functions depend on the isoform and cell type in which the PRL-receptor is engaged [15,17,18]. For instance, PRL promotes the proliferation, differentiation, and survival of mammary glands through JAK-STAT5 and PI3K-AKT signaling [19], while it activates STAT1 and STAT5 in endometrial cells [20].…”

Section: Introductionmentioning

confidence: 99%

Prolactin Rescues Immature B Cells from Apoptosis-Induced BCR-Aggregation through STAT3, Bcl2a1a, Bcl2l2, and Birc5 in Lupus-Prone MRL/lpr Mice

Flores-Fernández

Aponte-López

Suárez-Arriaga

et al. 2021

Cells

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Self-reactive immature B cells are eliminated through apoptosis by tolerance mechanisms, failing to eliminate these cells results in autoimmune diseases. Prolactin is known to rescue immature B cells from B cell receptor engagement-induced apoptosis in lupus-prone mice. The objective of this study was to characterize in vitro prolactin signaling in immature B cells, using sorting, PCR array, RT-PCR, flow cytometry, and chromatin immunoprecipitation. We found that all B cell maturation stages in bone marrow express the prolactin receptor long isoform, in both wild-type and MRL/lpr mice, but its expression increased only in the immature B cells of the latter, particularly at the onset of lupus. In these cells, activation of the prolactin receptor promoted STAT3 phosphorylation and upregulation of the antiapoptotic Bcl2a1a, Bcl2l2, and Birc5 genes. STAT3 binding to the promoter region of these genes was confirmed through chromatin immunoprecipitation. Furthermore, inhibitors of prolactin signaling and STAT3 activation abolished the prolactin rescue of self-engaged MRL/lpr immature B cells. These results support a mechanism in which prolactin participates in the emergence of lupus through the rescue of self-reactive immature B cell clones from central tolerance clonal deletion through the activation of STAT3 and transcriptional regulation of a complex network of genes related to apoptosis resistance.

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“…During sexual arousal, the afferent stimuli perceived in the pelvic area, the eyes, and the ear converge in the medial preoptic area and the arcuate nucleus, located in the hypothalamus, which maintains this state of arousal and induces prolactin secretion (PRL) and testosterone by the testis. 2,25 These hormones increase in the blood and bind to receptors located both in the testicle and in the prostate to complete sperm maturation and the production of prostate fluid that constitutes approximately one-third of the total ejaculated volume. Thus, seminal or ejaculate plasma comprises sperm from the testis and secretions from the seminal vesicles (for example, the seminogelin), the cooper's glands (for example, glycoprotein mucin 1 or MG1), and the prostate.…”

Section: Functionmentioning

confidence: 99%

“…2,43,44 In addition to this, the consistent execution of sexual behavior increases the volume and weight of the prostate, alveolar area, and epithelial height and the demand for prostatic fluid synthesis. For this, both hormones participate by capturing zinc, producing citrate, PSA and inducing a significant increase in cathepsin D. 17,25,29,45 The direct importance of all this is that the components of seminal plasma participate in events that are key in the function of sperm and fertilization, one of them is the liquefaction of seminal plasma. The other is sperm capacitation and activation.…”

Section: Endocrine Regulation Of the Prostatementioning

confidence: 99%

A pelvic trinity: prostate, hormones and nerves

Cruz-Rivas

Manzo²,

Rojas-Durán³

et al. 2022

MARJ

Self Cite

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The prostate is an accessory sex gland responsible for producing and excreting prostate fluid. In the male rat, hormones such as testosterone (T) and prolactin (PRL) and the pelvic and hypogastric nerves regulate the gland, providing afferent information and adrenergic and cholinergic innervation to the prostate. Damages in the innervation or alterations in the hormonal levels of T and PRL changes the prostate’s cytoarchitecture and function that can promote the presence of cancer. However, sexual activity delays effects induced by hormonal alterations or dysfunction of the autonomic nervous system, but it does not mean that they do not appear since the cases of death from prostate cancer is still increasing. That is why this review has the fundamental purpose of showing the relationship between the hormones, autonomic nervous system, and sexual behavior in the pathophysiology of the prostate, with the ultimate aim of trying to understand the role that each one plays in diseases of the prostate. To date, results show that morphological changes in the prostate correlate with an increase in prolactin serum levels, a decrease in androgen and long prolactin receptors, and an increase in short prolactin receptors. Also, damage in the innervation induces an increase in androgen and muscarinic receptors in the major pelvic ganglia that supply the nerves that control the prostate in animal with sexual experience.

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Effect of hyperprolactinemia on PRL-receptor expression and activation of Stat and Mapk cell signaling in the prostate of long-term sexually-active rats

Cited by 13 publications

References 50 publications

The prostate response to prolactin modulation in adult castrated rats subjected to testosterone replacement

The prostate response to prolactin modulation in adult castrated rats subjected to testosterone replacement

Prolactin Rescues Immature B Cells from Apoptosis-Induced BCR-Aggregation through STAT3, Bcl2a1a, Bcl2l2, and Birc5 in Lupus-Prone MRL/lpr Mice

A pelvic trinity: prostate, hormones and nerves

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