References of "Molecular & Cellular Endocrinology"
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See detailNeuroendocrine disruption of pubertal timing and interactions between homeostasis
Bourguignon, Jean-Pierre ULg; rasier, Gregory; Lebrethon, Marie-Christine ULg et al

in Molecular & Cellular Endocrinology (2010), 324(1-2), 110-120

The involvement of environmental factors such as endocrine disrupting chemicals (EDCs) in the timing of onset of puberty is suggested by recent changes in age at onset of puberty and pattern of ... [more ▼]

The involvement of environmental factors such as endocrine disrupting chemicals (EDCs) in the timing of onset of puberty is suggested by recent changes in age at onset of puberty and pattern of distribution that are variable among countries, as well as new forms of sexual precocity after migration. However, the evidence of association between early or late pubertal timing and exposure to EDCs is weak in humans, possibly due to heterogeneity of effects likely involving mixtures and incapacity to assess fetal or neonatal exposure retrospectively. The neuroendocrine system which is crucial for physiological onset of puberty is targeted by EDCs. These compounds also act directly in the gonads and peripheral sex-steroid sensitive tissues. Feedbacks add to the complexity of regulation so that changes in pubertal timing caused by EDCs can involve both central and peripheral mechanisms. In experimental conditions, several neuroendocrine endpoints are affected by EDCs though only few studies including from our laboratory aimed at EDC involvement in the pathophysiology of early sexual maturation. Recent observations support the concept that EDC cause disturbed energy balance and account for the obesity epidemic. Several aspects are linking this system and the reproductive axis: coexisting neuroendocrine and peripheral effects, dependency on fetal/neonatal programming and the many factors cross-linking the two systems, for instance leptin, adiponectin, Agouti Related Peptide (AgRP). This opens perspectives for future research and, hopefully, measures preventing the disturbances of homeostasis caused by EDCs. [less ▲]

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See detailRole of hormone cofactors in the human papillomavirus-induced carcinogenesis of the uterine cervix
Delvenne, Philippe ULg; Herman, Ludivine ULg; Kholod, Natalia et al

in Molecular & Cellular Endocrinology (2007), 264(1-2), 1-5

If human papillomavirus (HPV) is necessary for the development of (pre)neoplastic lesions of the uterine cervix, it is not sufficient. Among the cofactors involved in the malignant transformation of cells ... [more ▼]

If human papillomavirus (HPV) is necessary for the development of (pre)neoplastic lesions of the uterine cervix, it is not sufficient. Among the cofactors involved in the malignant transformation of cells infected by HPV, sex hormones may facilitate the cervical carcinogenesis by different mechanisms, including the induction of squamous metaplasia in the transformation zone of the cervix, interactions between steroid hormones and HPV gene expression and alterations of the local immune microenvironment. [less ▲]

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See detailFemale sexual maturation and reproduction after prepubertal exposure to estrogens and endocrine disrupting chemicals: A review of rodent and human data
Rasier, Gregory; Toppari, Jorma; Parent, Anne-Simone ULg et al

in Molecular & Cellular Endocrinology (2006), 254-255

Natural hormones and some synthetic chemicals spread into our surrounding environment share the capacity to interact with hormone action and metabolism. Exposure to such compounds can cause a variety of ... [more ▼]

Natural hormones and some synthetic chemicals spread into our surrounding environment share the capacity to interact with hormone action and metabolism. Exposure to such compounds can cause a variety of developmental and reproductive detrimental abnormalities in wildlife species and, potentially, in human. Many experimental and epidemiological data have reported that exposure of the developing fetus or neonate to environmentally relevant concentrations of some among these endocrine disrupters induces morphological, biochemical and/or physiological disorders in brain and reproductive organs, by interfering with the hormone actions. The impact of such exposures on the hypothalamic-pituitary-gonadal axis and subsequent sexual maturation is the subject of the present review. We will highlight epidemiological human studies and the effects of early exposure during gestational, perinatal or postnatal life in female rodents. (c) 2006 Elsevier Ireland Ltd. All rights reserved. [less ▲]

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See detailEGF stimulates Pit-1 independent transcription of the human prolactin pituitary promoter in human breast cancer SK-BR-3 cells through its proximal AP-1 response element
Manfroid, Isabelle ULg; Van de Weerdt, Cécile ULg; Baudhuin, Ariane et al

in Molecular & Cellular Endocrinology (2005), 229(1-2), 127-39

Normal and neoplastic human mammary gland cells are targets for the proliferative action of prolactin. These cells also synthesize prolactin, thereby inducing an autocrine/paracrine proliferative loop. We ... [more ▼]

Normal and neoplastic human mammary gland cells are targets for the proliferative action of prolactin. These cells also synthesize prolactin, thereby inducing an autocrine/paracrine proliferative loop. We present the first extensive analysis of the transcriptional regulation of the human prolactin gene (hPRL) in human mammary tumor cells, SK-BR-3. We show that the pituitary promoter is functional in these cells in the absence of the pituitary-specific factor Pit-1. Expression of exogenous Pit-1 or epidermal growth factor (EGF) treatment stimulates the transfected hPRL pituitary promoter and the endogenous hPRL expression. EGF stimulation is mediated by increased synthesis of c-fos and c-jun, resulting in AP-1 binding to the proximal hPRL pituitary promoter. This regulation involves the EGF receptor, possibly ErbB2 that is highly expressed in SK-BR-3 cells, and a PI3K/JNK pathway. The stimulation of hPRL gene transcription by EGF in mammary cells may include hPRL in a complex regulatory network controlling growth of human mammary cells. [less ▲]

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See detailEvidence of rainbow trout prolactin interaction with its receptor through unstable homodimerisation.
Le Rouzic, Philippe; Sandra, Olivier; Grosclaude, Jeanne et al

in Molecular & Cellular Endocrinology (2001), 172(1-2), 105-13

This study aims to characterise Prolactin receptor (PRLR) in rainbow trout for which no information is available despite the availability of Salmonid PRL preparations. By screening a freshwater rainbow ... [more ▼]

This study aims to characterise Prolactin receptor (PRLR) in rainbow trout for which no information is available despite the availability of Salmonid PRL preparations. By screening a freshwater rainbow trout intestine cDNA library with a probe corresponding to the extracellular domain (ECD) of tilapia PRLR, we have cloned a 2.5 kb insert coding for the PRLR. The mature protein of 614 amino acid residues is similar to PRLR isolated in tilapia and also the long form of mammalian PRLR. Analysis of PRLR gene expression in osmoregulatory organs revealed the presence of a unique transcript, thus confirming the involvement of this hormone in the control of osmoregulation in this fish species. By using surface plasmon resonance (SPR) technology, kinetic measurement of interaction between trout PRL and its receptor ECD was studied. This approach allowed us to demonstrate the formation of a transient, unstable homodimeric complex. This unstability could explain the inability to perform binding experiments using homologous PRL. In contrast, heterologous lactogenic ligands were able to interact through a more stable complex. Whether these characteristics of PRL-receptor interaction in rainbow trout are different to what occurs in tilapia where a homologous radioreceptor assay was developed would require further studies. [less ▲]

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See detailPit-1 mediates cell-specific and cAMP-induced transcription of the tilapia GH gene
Sekkali, B.; Belayew, A.; Bortolussi, M. et al

in Molecular & Cellular Endocrinology (1999), 152(1-2), 111-23

Expression of the tilapia growth hormone (tiGH) gene is pituitary-specific and controlled by intracellular cAMP levels. DNaseI protection experiments allowed us to identify four Pit-1 binding sites in the ... [more ▼]

Expression of the tilapia growth hormone (tiGH) gene is pituitary-specific and controlled by intracellular cAMP levels. DNaseI protection experiments allowed us to identify four Pit-1 binding sites in the tiGH - 465/ + 19 region. Deletion and mutagenesis analysis revealed that the - 131/+ 19 region, containing two Pit-1 sites, or four copies of the most proximal site tiGHF1 fused to the heterologous Tk promoter, confer high level expression in rat pituitary cells and direct transcription in non-pituitary cells only after expression of rat Pit-1. We show that a tilapia pituitary factor specifically binds to site tiGHF1 and obtained a partial cDNA sequence coding for tilapia Pit-1. The cAMP stimulation is mediated by the proximal (- 131/- 31) promoter region. It is Pit-1-dependent and requires the tiGHF1 site. In addition, four copies of this site confer cAMP inducibility to the Tk promoter in GC cells. [less ▲]

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See detailThe glucocorticoid receptor inhibits the human prolactin gene expression by interference with Pit-1 activity
Nalda, Asunción M; Martial, Joseph ULg; Muller, Marc ULg

in Molecular & Cellular Endocrinology (1997), 134(2), 129-37

Glucocorticoids have been shown to inhibit the activity of the human prolactin (hPRL) promoter. Using transient expression experiments in rat pituitary cells, we located the sequence conferring ... [more ▼]

Glucocorticoids have been shown to inhibit the activity of the human prolactin (hPRL) promoter. Using transient expression experiments in rat pituitary cells, we located the sequence conferring glucocorticoid inhibition to a region which contains Pit-1 binding sites, responsible for pituitary-specific expression, but does not seem to contain a glucocorticoid receptor (GR) binding site. Co-transfection experiments in non-pituitary cell lines, using expression vectors for Pit-1 and different mutants of the human GR show that inhibition of the hPRL gene is seen only in the presence of Pit-1 and GR, and that the DNA binding function of the receptor is not required. Immunoprecipitation studies show that either anti-GR or anti-Pit-1 antibodies are able to co-precipitate GR and Pit-1, suggesting an interaction between these factors. We conclude that the activated GR functionally interferes with the pituitary specific factor Pit-1, thereby leading to the observed transcriptional repression. [less ▲]

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See detailThyrotropin-releasing hormone and epidermal growth factor induce human prolactin expression via identical multiple cis elements
Berwaer, Monique; Peers, Bernard ULg; Nalda, Asuncion M et al

in Molecular & Cellular Endocrinology (1993), 92(1), 1-7

Pituitary GH3 cells were transfected with different deletion mutants of the human prolactin (hPRL) promoter fused to the CAT reporter gene. The proximal region (-250 to -42) was sufficient to confer ... [more ▼]

Pituitary GH3 cells were transfected with different deletion mutants of the human prolactin (hPRL) promoter fused to the CAT reporter gene. The proximal region (-250 to -42) was sufficient to confer stimulation by both thyrotropin-releasing hormone (TRH) and epidermal growth factor (EGF). Further deletion analyses demonstrated the importance of the three proximal Pit-1 binding sites in this response. However, Pit-1 binding oligonucleotides confer neither TRH nor EGF induction to a linked neutral promoter, suggesting that other elements might be involved. We have previously shown that sequence A (-115 to -85) is needed together with Pit-1 binding sites for full cyclic AMP response of hPRL-CAT. Mutation of this sequence strongly affects TRH and EGF induction. On the other hand, three copies of sequence A confer both TRH and EGF response to a linked neutral promoter. In conclusion, although TRH and EGF activate mostly different intracellular pathways, they mediate transcriptional induction of the hPRL promoter via identical cis elements. [less ▲]

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See detailSYNCYTIOTROPHOBLASTIC LOCALIZATION OF THE HUMAN GROWTH-HORMONE VARIANT MESSENGER-RNA IN THE PLACENTA
Scippo, Marie-Louise ULg; Frankenne, Francis ULg; HOOGHEPETERS, ELisabeth et al

in Molecular & Cellular Endocrinology (1993), 92(2), 7-13

The hGH/hCS genes, clustered on chromosome 17 in the 5' to 3' order GH-N, CS-L, CS-A, GH-V and CS-B, show a high degree of sequence identity. The expression product of the GH-V gene is the placental ... [more ▼]

The hGH/hCS genes, clustered on chromosome 17 in the 5' to 3' order GH-N, CS-L, CS-A, GH-V and CS-B, show a high degree of sequence identity. The expression product of the GH-V gene is the placental growth hormone, which replaces pituitary GH in maternal blood throughout pregnancy. By means of mRNA competitive hybridization using P-32-labelled and unlabelled 30 bases long oligonucleotides, we first optimized specific hybridization conditions. In situ hybridization was then performed to locate the GH-V mRNA encoding placental growth hormone. The hGH-V gene appears expressed in the placental syncytiotrophoblast. Unlike the CS-A and CS-B genes (both encoding hPL) which are expressed uniformly in the syncytiotrophoblast, the GH-V mRNA is located in a few syncytiotrophoblast cells only. [less ▲]

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See detailGrowth hormone and prolactin stimulate androgen receptor, insulin-like growth factor-I (IGF-I) and IGF-I receptor levels in the prostate of immature rats.
Reiter, E.; Bonnet, Pierre ULg; Sente, B. et al

in Molecular & Cellular Endocrinology (1992), 88(1-3), 77-87

In this study we investigated the involvement of several different pituitary hormones on rat prostate development. 22-day-old Wistar rats, hypophysectomized (hypox) at 19 days of age were supplemented ... [more ▼]

In this study we investigated the involvement of several different pituitary hormones on rat prostate development. 22-day-old Wistar rats, hypophysectomized (hypox) at 19 days of age were supplemented with highly purified human prolactin (hPRL), human luteinizing hormone (hLH), porcine follicle-stimulating hormone (pFSH), and bovine growth hormone (bGH) or with saline. Quantitative analysis of RNAs shows that treatment with either PRL or GH increases significantly steady-state mRNAs levels of the following genes in the prostate: androgen receptor (AR) (respectively 3.5- and 4.8-fold above hypox controls), IGF-I (5- and 2.7-fold), and IGF-I receptor (2.9- and 2.3-fold). LH and FSH, by contrast, have negative effects on these parameters. To test whether the enhancing effect of PRL and GH on AR-mRNA abundance was followed by increased content in the protein itself, binding assays were performed with the androgen agonist [3H]R1881 (131 and 153 fmol/mg protein while hypox controls contained 110 fmol/mg protein). In addition to the well-documented presence of prolactin receptors in prostatic tissues, we have further demonstrated, by means of nuclease S1 protection assays plus dot- and Northern-blot analyses, that a GH receptor mRNA is produced in the immature rat prostate. Moreover, we observed not only strong lactogenic but also purely somatogenic binding to be occurring in the immature prostates. Finally, we have studied IGF-I mRNA content in separated epithelial/stromal cell fractions and have concluded that IGF-I expression is principally located in the prostatic stroma. Taken together, these results suggest that PRL and GH are involved in regulating AR synthesis, at least partially by direct action on the organ. In this context IGF-I appears as a paracrine factor playing a role in epithelium/stroma interactions during prostatic development. [less ▲]

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See detailAt the Cutting Edge. Biosynthesis and Paracrine/Cryptocrine Actions of 'Self' Neurohypophysial-Related Peptides in the Thymus
Geenen, Vincent ULg; Robert, F.; Martens, Henri ULg et al

in Molecular & Cellular Endocrinology (1991), 76(1-3), 27-31

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See detailMultihormonal regulation of the human prolactin gene expression from 5000 bp of its upstream sequence
Berwaer, M.; Monget, P.; Peers, Bernard ULg et al

in Molecular & Cellular Endocrinology (1991), 80(1-3), 53-64

We have cloned DNA sequences extending up to 6000 bp upstream from the first exon of the human prolactin (hPRL) gene. 5000 bp of these upstream sequences were fused to a CAT reporter gene and shown to ... [more ▼]

We have cloned DNA sequences extending up to 6000 bp upstream from the first exon of the human prolactin (hPRL) gene. 5000 bp of these upstream sequences were fused to a CAT reporter gene and shown to provide tissue-specific transient expression in rat pituitary GH3 cells. Multihormonal response was found in this transient expression assay, leading to significant 2- to 5-fold induction by addition of 8-chlorophenylthio-cyclic AMP, thyrotropin-releasing hormone, epidermal growth factor, basic fibroblast growth factor, phorbol myristate acetate, a calcium channel agonist (Bay K-8644) and triiodothyronine. A 3-fold inhibition was observed in the presence of the glucocorticoid agonist dexamethasone. The sequence of the hPRL promoter was determined up to coordinate -3470. Computer similarity search between the rat and human sequences showed two highly conserved regions corresponding to the proximal and distal tissue specific enhancers described in both PRL promoters. [less ▲]

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See detailTriiodothyronine inhibits transcription from the human growth hormone promoter
Morin, A.; Louette, J.; Voz, Marianne ULg et al

in Molecular & Cellular Endocrinology (1990), 71(3), 261-7

Three DNA constructs, the natural human growth hormone gene (hGH-hGH) its 500 bp promoter linked to the chloramphenicol acetyl transferase reporter gene (hGH-CAT), and its structural part linked to the ... [more ▼]

Three DNA constructs, the natural human growth hormone gene (hGH-hGH) its 500 bp promoter linked to the chloramphenicol acetyl transferase reporter gene (hGH-CAT), and its structural part linked to the herpes virus thymidine kinase promoter (TK-hGH) were introduced into rat pituitary GC cells by DEAE-dextran transfection. Transient expression was followed as a function of triiodothyronine (T3) concentration. The hGH-CAT expression was specifically inhibited by T3 following a typical dose-response curve while hGH-GH gene expression was not significantly modified. The transient expression of TK-hGH increased as a function of T3 concentration. These results indicate that T3 exerts two opposite effects on hGH gene expression. First, it down-regulates expression by acting on the promoter; second, it up-regulates expression by acting on the structural part of the gene. These action could be due to regulation of transcription and mRNA stabilization, respectively. [less ▲]

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