MMQ cells: a model for evaluating the role of g proteins in the modulation of prolactin release

Forget, Hélène; Painson, Jean-Claude; Drews, Roman; Lagacé, Ginette; Collu, R.

doi:10.1016/0303-7207(93)90115-z

Cited by 10 publications

(4 citation statements)

References 55 publications

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“…Not all clonal lactotroph lines deviate as markedly from primary cells. For example, the MMQ cell line derived from the estrogen-induced rat pituitary tumor 7315a secretes prolactin exclusively, expresses functional dopamine D 2 receptors (881), and behaves in a manner similar to (but not the same as) that of normal lactotrophs (567,699).…”

Section: F Prolactin-secreting Cell Linesmentioning

confidence: 99%

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

et al. 2007

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Hyperprolactinemia can reduce fertility and libido. Although central prolactin actions are thought to contribute to this, the mechanisms are poorly understood. We first tested whether chronic hyperprolactinemia inhibited two neuroendocrine parameters necessary for female fertility: pulsatile LH secretion and the estrogen-induced LH surge. Chronic hyperprolactinemia induced by the dopamine antagonist sulpiride caused a 40% reduction LH pulse frequency in ovariectomized rats, but only in the presence of chronic low levels of estradiol. Sulpiride did not affect the magnitude of a steroid-induced LH surge or the percentage of GnRH neurons activated during the surge. Estradiol is known to influence expression of the long form of prolactin receptors (PRL-R) and components of prolactin's signaling pathway. To test the hypothesis that estrogen increases PRL-R expression and sensitivity to prolactin, we next demonstrated that estradiol greatly augments prolactin-induced STAT5 activation. Lastly, we measured PRL-R and suppressor of cytokine signaling (SOCS-1 and -3 and CIS, which reflect the level of prolactin signaling) mRNAs in response to sulpiride and estradiol. Sulpiride induced only SOCS-1 in the medial preoptic area, where GnRH neurons are regulated, but in the arcuate nucleus and choroid plexus, PRL-R, SOCS-3, and CIS mRNA levels were also induced. Estradiol enhanced these effects on SOCS-3 and CIS. Interestingly, estradiol also induced PRL-R, SOCS-3, and CIS mRNA levels independently. These data show that GnRH pulse frequency is inhibited by chronic hyperprolactinemia in a steroid-dependent manner. They also provide evidence for estradiol-dependent and brain region-specific regulation of PRL-R expression and signaling responses by prolactin.

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Section: F Prolactin-secreting Cell Linesmentioning

confidence: 99%

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

et al. 2007

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“…MMQ, a rat pituitary cell line (14,15), was grown in RPMI medium 1640 supplemented with 10% fetal calf serum and 5% horse serum. Time course induction assays with all-trans-RA (t-RA) and 9-cis-RA at 0.1 M were performed in RPMI medium 1640 supplemented with charcoal-treated serum.…”

Section: Methodsmentioning

confidence: 99%

Regulation of dopaminergic pathways by retinoids: Activation of the D2 receptor promoter by members of the retinoic acid receptor–retinoid X receptor family

Samad

Krężel

Chambon

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

208

133

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Dopamine is a neuromodulator involved in the control of key physiological functions. Dopaminedependent signal transduction is activated through the interaction with membrane receptors of the seven-transmembrane domain G protein-coupled family. Among them, dopamine D2 receptor is highly expressed in the striatum and the pituitary gland as well as by mesencephalic dopaminergic neurons. Lack of D2 receptors in mice leads to a locomotor parkinsonian-like phenotype and to pituitary tumors. The D2 receptor promoter has characteristics of a housekeeping gene. However, the restricted expression of this gene to particular neurons and cells points to a strict regulation of its expression by cell-specific transcription factors. We demonstrate here that the D2 receptor promoter contains a functional retinoic acid response element. Furthermore, analysis of retinoic acid receptor-null mice supports our finding and shows that in these animals D2 receptor expression is reduced. This finding assigns to retinoids an important role in the control of gene expression in the central nervous system.

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“…In the case of the D 2 receptor, the situation has not been so clear to date. More importantly, the very low levels of D 2 receptors and coupled G proteins that are detected in MMQ cells (13) do not allow easy detection of functional changes depending on D 2 receptor splicing in this cell model. Accordingly, Guiramand et al (32) showed that the long isoform of the D 2 receptor is preferentially able to activate G i2 protein, whereas the short isoform could be more efficient for G protein activation in cells that do not express G i2 (33).…”

Section: Discussionmentioning

confidence: 95%

Alternative Splicing of the D₂Dopamine Receptor Messenger Ribonucleic Acid Is Modulated by Activated Sex Steroid Receptors in the MMQ Prolactin Cell Line¹

Guivarc'h¹,

Vincent²,

Vernier³

1998

Endocrinology

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The two isoforms of the D2 dopamine receptor are generated by alternative splicing of the exon 6 of the premessenger RNA (pre-mRNA), changing the length of the third cytoplasmic loop involved in the coupling to G proteins. In the MMQ PRL cell line, sex steroid hormones modulated the proportion of the two D2 receptor isoforms. Under controlled culture conditions, 17beta-estradiol (E2) strongly favored the production of the long isoform of D2 mRNA over the short one, whereas both isoforms were equally abundant when culture medium was hormone depleted. In the presence of progesterone (P), E2 action was inhibited, and equal amounts of each D2 receptor isoform were produced in the cells. Hormone treatments never modified either the total amount of D2 receptor mRNA and D2 receptor binding sites or D2 receptor-mediated inhibition of adenylyl cyclase. Specific antagonists demonstrated that the activity of each hormone depended on their nuclear receptors. Inhibitors of gene transcription or translation also showed that their activity required protein synthesis. The expression of the short D2 receptor isoform was never prominent, even at the single cell level. Analysis of the intron sequence flanking alternative exon 6 showed that only the upstream intron presented two sequence tracts known to be targets for splicing factors. Taken together, these results provide converging evidence for a physiologically relevant mechanism by which sex steroid receptors could regulate the expression of a splicing factor favoring the production of the long dopamine D2 receptor isoform.

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MMQ cells: a model for evaluating the role of g proteins in the modulation of prolactin release

Cited by 10 publications

References 55 publications

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

Regulation of dopaminergic pathways by retinoids: Activation of the D2 receptor promoter by members of the retinoic acid receptor–retinoid X receptor family

Alternative Splicing of the D₂Dopamine Receptor Messenger Ribonucleic Acid Is Modulated by Activated Sex Steroid Receptors in the MMQ Prolactin Cell Line¹

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MMQ cells: a model for evaluating the role of g proteins in the modulation of prolactin release

Cited by 10 publications

References 55 publications

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

Regulation of dopaminergic pathways by retinoids: Activation of the D2 receptor promoter by members of the retinoic acid receptor–retinoid X receptor family

Alternative Splicing of the D2Dopamine Receptor Messenger Ribonucleic Acid Is Modulated by Activated Sex Steroid Receptors in the MMQ Prolactin Cell Line1

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Alternative Splicing of the D₂Dopamine Receptor Messenger Ribonucleic Acid Is Modulated by Activated Sex Steroid Receptors in the MMQ Prolactin Cell Line¹