Secretion of Alpha Subunits of Luteinizing Hormone (LH) by the Anterior Pituitary

Edmonds, M.; Molitch, Matthew; Pierce, John G.; Odell, William D.

doi:10.1210/jcem-41-3-551

Cited by 65 publications

(9 citation statements)

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“…Functional interspecies hybrid molecules have been produced between human and bovine glycoprotein hormone subunits (42,47) but have not been reported for human and mouse subunits. If functional hybrid molecules are produced in our transgenic mice, the absence of abnormalities may not be unusual given that the alpha subunit is normally synthesized in excess of the glycoprotein hormone beta subunits in the pituitary (16,30,31,40,46). Beta-subunit synthesis is thus believed to be rate limiting in the production of functional hormone (17,21,43).…”

Section: Discussionmentioning

confidence: 99%

Expression and regulation of the pituitary- and placenta-specific human glycoprotein hormone alpha-subunit gene is restricted to the pituitary in transgenic mice.

Fox¹,

Solter²

1988

Mol. Cell. Biol.

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Expression of the glycoprotein hormone alpha subunit occurs in both the pituitary and placenta in humans. However, this study found that expression of this subunit is restricted to the pituitary in mice. An interspecies analysis of human alpha-subunit gene regulation was undertaken, using the transgenic-mouse approach. In mice transgenic for a genomic clone containing the complete human alpha-subunit gene and several kilobases of 5'- and 3'-flanking sequences, cell-type-specific expression and hormonal regulation of the human alpha-subunit transgene occurred in the mouse pituitary, whereas no expression of the transgene was detectable in the mouse placenta. These findings provide strong evidence that a common trans-acting factor(s) regulates glycoprotein hormone alpha-subunit gene expression in the human and mouse pituitaries; however, this factor(s) or a unique factor(s), though functional in the human placenta, is either nonfunctional or absent in the mouse placenta.

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Section: Discussionmentioning

confidence: 99%

Expression and regulation of the pituitary- and placenta-specific human glycoprotein hormone alpha-subunit gene is restricted to the pituitary in transgenic mice.

Fox¹,

Solter²

1988

Mol. Cell. Biol.

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“…However, it is known that GnRH induces the release of the free a-subunit together with the release of gonado tropins in humans [8]. A peak of a-subunit can be observed during the periovulatory period of the menstrual cycle con current with gonadotropin peak [20].…”

Section: Discussionmentioning

confidence: 99%

Prolactin-Releasing Action of a Low Dose of Exogenous Gonadotropin-Releasing Hormone Throughout the Human Menstrual Cycle

Mais¹,

Melis²,

Paoletti³

et al. 1986

Neuroendocrinology

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Pharmacological doses of gonadotropin-releasing hormone (GnRH) are known to induce prolactin (PRL) release in different pathological states. The same effect can be observed in postmenopausal women and during the phases of menstrual cycle characterized by high estrogen levels. With the aim to evaluate whether nonpharmacological doses of GnRH are also able to induce PRL release, gonadotropin and PRL response to a low dose of GnRH (10 µg, i.v. bolus) was evaluated in 70 normal women during different phases of their menstrual cycle. A significant PRL increase was observed in 33% of subjects during the first days of the cycle (menstrual phase; days 1–3 from the beginning of menstrual bleeding; n = 6), in 24% of subjects during early follicular phase (days – 10 to -8 from LH peak; n= 17); in 38% of subjects during midfollicular phase (days – 6 to – 4 from LH peak; n = 8); in 78% of subjects during preovulatory phase (days – 2 to – 1 from LH peak; n = 9); in 67% of subjects during postovulatory phase (days + 1 to +2 from LH peak; n = 6) and in 42% of subjects during midluteal phase (days +5 to +8 from LH peak; n = 24). In brief, the increase of mean PRL levels after GnRH administration was only significant (p < 0.05) during pre- and postovulatory phases. The percentage of patients who showed a PRL response during the different phases of menstrual cycle was significantly correlated to the mean maximal net increase of LH (r = 0.927; p < 0.01) and to the mean maximal net increase of FSH (r = 0.926; p < 0.01). In conclusion, the present data show that in normal cycling women the administration of exogenous GnRH induces PRL release even at low doses. The PRL-releasing effect of GnRH is variable throughout the menstrual cycle and it is maximal during the periovulatory period. The significant correlation between PRL release and gonadotrophs responsiveness to GnRH suggests that a paracrine interaction between gonadotrophs and lactotrophs might exist also in humans.

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“…There are several lines ofevidence suggesting dysregulation ofgonadotropin and free subunit secretion by gonadotropin-releasing hor-lates gonadotropin secretion in normal individuals (3). In contrast, < 50% of patients with gonadotropin-secreting tumors exhibit in vivo increases in serum levels of intact gonadotropins and free subunits after an intravenous bolus ofGnRH (4,5).…”

Section: Introductionmentioning

confidence: 99%

Gonadotropin-releasing hormone receptor mRNA expression by human pituitary tumors in vitro.

Alexander

Klibanski²

1994

J. Clin. Invest.

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An important question in the pathogenesis and regulation of human gonadotroph adenomas is whether heterogeneous gonadotropin responses to gonadotropin-releasing hormone (GnRH) are due to dysregulation of GnRH receptor biosynthesis and/ or cell-signaling pathways. We investigated gonadotropin responsiveness to pulsatile GnRH in 13 gonadotroph adenomas. All tumors had evidence of follicle-stimulating hormone (FSH) ft and a subunit biosynthesis using reverse transcriptase/polymerase chain reaction (RTPCR) techniques. Four tumors significantly increased gonadotropin and/or free subunit secretion during pulsatile 10-8 M GnRH administration. The GnRH antagonist Antide (10-' to 108 M) blocked secretory increases in all GnRH-responsive tumors. Gonadotropin and/or free subunit secretion increased after 60 mM KCl, confirming that GnRH nonresponsiveness was not due to intracellular gonadotropin depletion. We hypothesized that GnRH nonresponsiveness in these tumors may be due to GnRH receptor (GnRHRc) biosynthetic defects. RTPCR analyses detected GnRH-Rc transcripts only in responsive tumors and normal human pituitary. This is the first demonstration of a cell-surface receptor biosynthetic defect in human pituitary tumors. We conclude (a) one third of gonadotroph tumors respond to pulsatile GnRH in vitro, (b) GnRH-Rc mRNA is detected in human gonadotroph adenomas and predicts GnRH responsiveness, and (c) GnRHRc biosynthetic defects may underlie GnRH nonresponsiveness in gonadotroph tumors. (J. Clin. Invest. 1994.93:2332-2339

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Secretion of Alpha Subunits of Luteinizing Hormone (LH) by the Anterior Pituitary

Cited by 65 publications

References 0 publications

Expression and regulation of the pituitary- and placenta-specific human glycoprotein hormone alpha-subunit gene is restricted to the pituitary in transgenic mice.

Expression and regulation of the pituitary- and placenta-specific human glycoprotein hormone alpha-subunit gene is restricted to the pituitary in transgenic mice.

Prolactin-Releasing Action of a Low Dose of Exogenous Gonadotropin-Releasing Hormone Throughout the Human Menstrual Cycle

Gonadotropin-releasing hormone receptor mRNA expression by human pituitary tumors in vitro.

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