Estrogen Regulates the Serum Level of Phosphorylated Prolactin in Mice

Horiguchi, Kotaro; Fukuta, Shinya; Yoshida, Makoto; Kosugi, Tatsuya; Naito, Jun-ichiro; Ishida, Michiyo; Harigaya, Toshio

doi:10.1262/jrd.18158

Cited by 6 publications

(2 citation statements)

References 23 publications

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“…The present study supports our hypothesis that an increased E:P ratio is very important for promoting effects on uterine carcinogenesis. There are a number of studies showing that PRL, E2 and/or their receptors control each other through endocrine and autocrine/paracrine mechanisms [34][35][36]. While the BRC treatment did not affect estrous cyclicity in the present study, the decrease in the serum E2: P ratio and tendency of the serum E2 levels to decrease might be related to the inhibitory effect on uterine cancer development.…”

Section: Discussioncontrasting

confidence: 64%

Long-Term Treatment with Bromocriptine Inhibits Endometrial Adenocarcinoma Development in Rats

Yoshida

Watanabe

Suzuki

et al. 2009

Journal of Reproduction and Development

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Abstract. The effects of long-term blockade of prolactin (PRL) action by bromocriptine (BRC) treatment on uterine carcinogenesis and on related ovarian physiology were investigated using a rat uterine cancer model. Ten-week-old cycling female Donryu rats, a high yield strain for uterine corpus tumors (endometrial adenocarcinomas), were treated with N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG), as a tumor initiator, and injected with 1 mg/kg body weight BRC subcutaneously 4 times per week until 14.5 months of age to block the proestrus PRL surge. The study was terminated at 15 months of age, and the results showed that long-term BRC treatment significantly inhibited endometrial adenocarcinoma development in terms of both incidence (34.6% to 13.0% with significant difference at 5%) and multiplicity (0.35 to 0.18 with significant difference at 5%), which indicates the number of adenocarcinomas per animals. While BRC did not affect estrous cyclicity in the treated animals, a significant decline was evident in the serum 17β-estradiol (E2) to progesterone (P) ratio (E: P ratio), and the serum E2 level showed a decreased tendency at 15 months of age. While the precise pathway to the inhibitory effect could not be determined; the pathway by which ovarian hormonal imbalance decreases the serum E: P ratio most likely plays a crucial role. Key words: Bromocripchne, Long-term treatment, Prolactin blockade, Rat, Uteirne carcinogenesis (J. Reprod. Dev. 55: [105][106][107][108][109] 2009) varian steroidhormone imbalance contributes to uterine carcinogenesis in human beings [1]. Maekawa et al. [2][3][4] have provided evidence that a similar imbalance, especially elevated 17β-estradiol (E2) levels relative to progesterone (P) levels (the E:P ratio), plays a crucial role in promoting endometrial adenocarcinoma development in rodents. While it is well-established that E2 and estrogenic chemicals play supportive or sometimes initiative roles in uterine carcinogenesis in rats as well as women, P may exert an inhibitory influence on human uterine cancer development [5][6][7]. However, the effects of other hormones related to the pituitary or ovaries on uterine carcinogenesis are not well known.Prolactin (PRL) is one of the important regulators of the corpus luteum as well as luteinizing hormone (LH), prostaglandin and vascular endothelial growth factors and platelet derived growth factors in rats [8][9][10]. The function of PRL as a luteotrophic and luteolytic hormone, however, is very complex [11][12][13][14][15][16][17]. Repeated injection of PRL has been shown to stimulate rapid regression of the persistent corpus luteum, with a concomitant decline in total steroidogenic capacity [12,18]. These studies indicate the possibility that the modulation of P production induced by PRL or its inhibitor affect uterine carcinogenesis through ovarian hormonal imbalance. On the other hand, PRL receptors, especially long-form ones (PRLR-L) [19], are present in the uteri of rats. PRL is known to play important roles in adenomyosis formation in ...

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Section: Discussioncontrasting

confidence: 64%

Long-Term Treatment with Bromocriptine Inhibits Endometrial Adenocarcinoma Development in Rats

Yoshida

Watanabe

Suzuki

et al. 2009

Journal of Reproduction and Development

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“…Indeed, as estradiol could have a stimulatory effect on prolactin secretion (Horiguchi et al . ; Saitoh et al . ; Avtanski et al .…”

Section: Discussionmentioning

confidence: 98%

Estradiol‐induced neurogenesis in the female accessory olfactory bulb is required for the learning of the male odor

Brus

Trouillet

Hellier

et al. 2016

Journal of Neurochemistry

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Odors processed by the main and accessory olfactory bulbs (MOB, AOB) are important for sexual behavior. Interestingly, both structures continue to receive new neurons during adulthood. A role for olfactory neurogenesis in sexual behavior in female mice has recently been shown and gonadal hormones such as estradiol can modulate adult neurogenesis. Therefore, we wanted to determine the role of estradiol in learning the odors of sexual partners and in the adult neurogenesis of female aromatase knockout mice (ArKO), unable to produce estradiol. Female wild-type (WT) and ArKO mice were exposed to male odors during 7 days, and olfactory preferences, cell proliferation, cell survival and functional involvement of newborn neurons were analyzed, using BrdU injections, in combination with a marker of cell activation (Zif268) and neuronal fate (doublecortin, NeuN).Behavioral tasks indicated that both WT and ArKO females were able to discriminate between the odors of two different males, but ArKO mice failed to learn the familiar male odor. Proliferation of newborn cells was reduced in ArKO mice only in the dentate gyrus of the hippocampus. Olfactory exposure decreased cell survival in the AOB in WT females, suggesting a role for estradiol in a structure involved in sexual behavior. Finally, newborn neurons do not seem to be functionally involved in the AOB of ArKO mice compared with WT, when females were exposed to the odor of a familiar male, suggesting that estradiol-induced neurogenesis in the AOB is required for the learning of the male odor in female mice.

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Paradigm-Shifters: Phosphorylated Prolactin and Short Prolactin Receptors

Huang

Ueda

Chen

et al. 2008

J Mammary Gland Biol Neoplasia

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Since the discovery of physiologically-regulated prolactin (PRL) phosphorylation, one focus of the laboratory has been an examination of the different functions of the unmodified and phosphorylated hormone. In the mammary gland, unmodified PRL promotes growth activities, whereas phosphorylated or pseudophosphorylated PRL antagonizes this while also being a superior agonist for changes that favor differentiation. Phosphorylated PRL also increases expression of the short forms of the PRL receptor. These short forms of the receptor have functions beyond the accepted dominant negative and in mammary epithelial cells are capable of generating an intracellular signal leading to increased tight junction formation and beta-casein expression.

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Estrogen Regulates the Serum Level of Phosphorylated Prolactin in Mice

Cited by 6 publications

References 23 publications

Long-Term Treatment with Bromocriptine Inhibits Endometrial Adenocarcinoma Development in Rats

Long-Term Treatment with Bromocriptine Inhibits Endometrial Adenocarcinoma Development in Rats

Estradiol‐induced neurogenesis in the female accessory olfactory bulb is required for the learning of the male odor

Paradigm-Shifters: Phosphorylated Prolactin and Short Prolactin Receptors

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