Modulation of Prolactin Expression by Xenoestrogens

Rousseau, Joël; Cossette, Louis; Grenier, Sonya; Martinoli, Maria-Grazia

doi:10.1006/gcen.2002.7789

Cited by 23 publications

(17 citation statements)

References 37 publications

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“…Recently, xenoestrogens have been reported to play a role in body growth and development, and BPA has been shown to influence the induction of PRL secretion [36,37]. E2 and certain xenoestrogens have been shown to modulate PRL expression, and exposure to EDs has been shown to increase PRL transcription significantly in a rat pituitary cell line [9]. These findings suggested that PRL is an estrogen responsive gene that could serve as an biomarker for assessing the estrogenicity of EDs.…”

Section: Discussionmentioning

confidence: 95%

“…Interactions between these ERs and estrogen responsive elements (ERE) in the promoters of many genes then leads to the regulation of gene expression [43]. Functionally, ERs mediate pituitary cell responsiveness to estrogens [28] and thus, estrogen may influence GH3 cell growth and increase PRL release [9]. In addition, co-treatment with ICI 182780 antagonizes E2-induced PRL secretion [44], suggesting that ERs play a physiological role in mediating PRL release.…”

Section: Discussionmentioning

confidence: 99%

“…E2 and certain xenoestrogens have been shown to modulate PRL expression, and exposure to EDs has been shown to increase PRL transcription significantly in a rat pituitary cell line [9]. These findings suggested that PRL is an estrogen responsive gene that could serve as an biomarker for assessing the estrogenicity of EDs.…”

Section: Effect Of Endocrine Disruptor On Induction Of Gh Expressionmentioning

confidence: 95%

“…Prolactin (PRL) is a growth promoting protein secreted from the pituitary gland that plays important roles in a variety of processes including growth, metabolism, reproduction, parental behavior and immune responses [9]. Cellular proliferation is considered to be a major function of PRL during body growth and development in mammals [10].…”

mentioning

confidence: 99%

“…Cellular proliferation is considered to be a major function of PRL during body growth and development in mammals [10]. In addition, it appears that PRL performs a wider range of activities than the other pituitary hormones, functioning as both a growth regulator and neurotransmitter [9]. PRL gene expression and secretion appear to be regulated by estradiol (E2).…”

mentioning

confidence: 99%

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Estrogen Receptors are Involved in Xenoestrogen Induction of Growth Hormone in the Rat Pituitary Gland

Dang

Choi

Jeung

2009

Journal of Reproduction and Development

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Abstract. Growth hormone (GH) plays a pivotal role in the regulation of growth, development and body composition. In order to provide new insights into estrogenic endocrine disruptor (ED) activities in the pituitary gland and the potential role played by estrogen receptors (ERs) in mediating their effects in vivo, we examined GH expression in the pituitary gland of an immature rat model. At postnatal day 14, immature rats were treated with various doses of 4-tertoctylphenol (OP), p-nonylphenol (NP) and bisphenol A (BPA), and the GH mRNA and protein expression levels were analyzed by real-time quantitative PCR and western blot/immunohistochemistry (IHC), respectively. An anti-estrogen (ICI 182780) was used to examine the potential involvement of ERs in ED-induced GH expression during critical windows of development. GH mRNA expression increased significantly 48 h after treatment with a high dose (600 mg/ kg body weight [BW]) of OP or NP. However, this induction was abolished completely by co-treatment with ICI 182780. No significant difference in GH mRNA expression was observed following treatment with BPA or co-treatment of BPA with the anti-estrogen. Exposure to high doses (600 mg/kg BW) of these EDs significantly enhanced GH protein expression in the rat pituitary gland, whereas pretreatment with ICI 182780 markedly reduced this expression. Taken together, we have demonstrated for the first time that in vivo exposure to EDs can induce GH mRNA and protein expression in the rat pituitary gland and that their activities may involve an ER-mediated signaling pathway. These results may provide critical evidence for ED-induced dysregulation of pituitary GH expression and thus may be important for elucidating the potential impacts of EDs in altered body growth and development and for predicting the health risks of ED exposure in humans and wildlife. Key words: Endocrine disruptor, Estrogenicity, Growth hormone, Pituitary gland, Rat (J. Reprod. Dev. 55: [206][207][208][209][210][211][212][213] 2009) rowth hormone (GH) plays a pivotal role in growth and development during puberty and is a member of a family of evolutionarily-related hormones that include prolactin (PRL) and placental lactogen [1]. In addition, GH performs important functions in metabolism and body composition [2]. GH activity can be regulated directly via sex steroids, which control GH release, or indirectly by modulation of insulin-like growth factor (IGF)-I [3]. Although most of its growth-promoting activity is mediated by IGF-I activation [1], studies have indicated that changes in circulating levels of sex steroids may lead to modulation of GH synthesis and release of GH from the anterior lobe of the pituitary [4]. In humans, GH regulates growth in childhood [5], and most endocrine disorders that influence body growth and development affect GH levels during this critical window. Recent reports have indicated a positive correlation between GH and estrogen levels in prepubertal girls and boys [6,7]. The effects of estrogen stimulation on growth dep...

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Section: Effect Of Endocrine Disruptor On Induction Of Gh Expressionmentioning

confidence: 95%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Estrogen Receptors are Involved in Xenoestrogen Induction of Growth Hormone in the Rat Pituitary Gland

Dang

Choi

Jeung

2009

Journal of Reproduction and Development

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Resveratrol and quercetin, two natural polyphenols, reduce apoptotic neuronal cell death induced by neuroinflammation

Bureau

Longpré

Martinoli

2007

J of Neuroscience Research

298

181

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Parkinson's disease (PD) is a movement disorder characterized by a progressive loss of nigrostriatal dopaminergic neurons. Microglia activation and neuroinflammation have been associated with the pathogenesis of PD. Indeed, cytokines have been proposed as candidates that mediate the apoptotic cell death of dopaminergic neurons seen in PD. In this study, we investigated the effect of two natural polyphenols, resveratrol and quercetin, on neuroinflammation. For glial cells, we observed that lipopolysaccharide (LPS)-induced mRNA levels of two proinflammatory genes, interleukin 1-alpha and tumor necrosis factor-alpha, are strongly decreased by treatments with resveratrol or quercetin. We also undertook microglial-neuronal coculture to examine the influence of resveratrol and quercetin on dopaminergic neuronal cell death evoked by LPS-activated microglia. Cytotoxicity assays were performed to evaluate the percentage of cell death, with apoptotic cells identified by both the TdT-mediated dUTP nick end labeling technique and the detection of cleaved caspase-3. We report that treatment of N9 microglial cells with resveratrol or quercetin successfully reduced the inflammation-mediated apoptotic death of neuronal cells in our coculture system. Altogether our results demonstrate that resveratrol and quercetin diminished apoptotic neuronal cell death induced by microglial activation and suggest that these two phytoestrogens may be potent antiinflammatory compounds.

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Dopamine D2 agonists, bromocriptine and quinpirole, increase MPP+-induced toxicity in PC12 cells

et al. 2006

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Dopaminergic cell loss in the mesencephalic substantia nigra is the hallmark of Parkinson's disease and may be associated with abnormal oxidative metabolic activity. However, the delicate balance underlying dopamine decline and oxidative stress is still a matter of debate. The aim of this study was to analyze the possible modulation of D2 agonists and antagonists on MPP+ (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridinium ion) -induced cellular death in differentiated and undifferentiated PC12 cells. Using colorimetric assays, western blots and reverse transcriptase-PCR, we demonstrated that two D2 agonists, bromocriptine and quinpirole, consistently increased MPP+ -induced cytotoxicity in both differentiated and undifferentiated PC12 cells, whereas D2 antagonists do not modulate cell death. However, this increase in cellular death was reversed when bromocriptine or quinpirole were used in presence of D2 antagonists. On the other hand, 1-{2-[bis-(4-fluorophenyl)methoxy]ethyl}-4-(3-phenylpropyl)piperazine (GBR 12909), a potent inhibitor of the dopamine transporter, partially reversed MPP+ -induced cellular death and completely abolished the increase of cellular death induced by bromocriptine. Dopamine agonists and antagonists also modulate the expression of the dopamine transporter in PC12 cells; in particular, bromocriptine may alter MPP+ uptake by increasing DAT expression We also show that, in our cellular paradigm, D2 receptor mRNA levels are more abundant that D3 mRNA levels and MPP+ and /or bromocriptine could not modulate D2 gene expression while D3 gene expression clearly decrease after MPP+ and /or bromocriptine treatment.

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Modulation of Prolactin Expression by Xenoestrogens

Cited by 23 publications

References 37 publications

Estrogen Receptors are Involved in Xenoestrogen Induction of Growth Hormone in the Rat Pituitary Gland

Estrogen Receptors are Involved in Xenoestrogen Induction of Growth Hormone in the Rat Pituitary Gland

Resveratrol and quercetin, two natural polyphenols, reduce apoptotic neuronal cell death induced by neuroinflammation

Dopamine D2 agonists, bromocriptine and quinpirole, increase MPP+-induced toxicity in PC12 cells

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