Anterior pituitary pyroglutamyl peptidase II activity controls TRH-induced prolactin release

Cruz, Raymundo; Vargas, Miguel; Uribe, R.M.; Pascual, Isel; Lazcano, Iván; Yiotakis, Athanasios; Matziari, Magdalini; Joseph‐Bravo, Patricia; Charlí, Jean-Louis

doi:10.1016/j.peptides.2008.07.011

Cited by 19 publications

(17 citation statements)

References 55 publications

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“…This observation reflects a specific regulation of PPII activity over TRH stimulation of lactotrophs or tyrotrophs depending on the physiological context of the animals, as has been previously suggested (Cruz et al, 2008). Increased PRL release is already described in lactating Zn‐deficient dams (Chowanadisai et al, 2004), although TSH concentration was not evaluated in that study.…”

Section: Discussionsupporting

confidence: 80%

Mediobasal hypothalamic and adenohypophyseal TRH‐degrading enzyme (PPII) is down‐regulated by zinc deficiency

Alvarez-Salas

Alcántara-Alonso

Matamoros-Trejo

et al. 2015

Intl J of Devlp Neuroscience

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Thyrotropin-releasing hormone (TRH) synthesized in hypothalamic paraventricular nucleus directs hypothalamus-pituitary-thyroid (HPT) axis function, regulating thyrotropin release from adenohypophysis and thyroid hormones serum concentration. Pyroglutamyl aminopeptidase II (PPII), a Zn-dependent metallopeptidase located in adenohypophysis and medial-basal-hypothalamus degrades TRH released from the median eminence and participates in HPT axis function by regulating TRH-induced thyrotropin release from adenohypophysis. It is unknown whether dietary Zn deficiency down-regulates PPII. Our aim was to compare adenohypohyseal and medial-basal-hypothalamic PPII activity and expression of adult rats fed a Zn-deficient diet (2ppm) throughout their lifespan (DD), prenatally (DC) or after weaning (CD) vs. that of animals fed a control diet (20ppm:CC). Female rats consumed a Zn-deficient or control diet from two weeks before gestation and up to the end of lactation. We analyzed adenohypophyseal and medial-basal-hypothalamic PPII activity of dams and male offspring when adults; its relation to median eminence TRH, serum thyrotropin, leptin and thyroid hormones concentration. Offspring ate the same diet as their dams (CC, DD) or were switched from dietary regime after weaning (CD, DC) and until 2.5 months of age. DD males showed decreased adenohypophyseal and medial-basal-hypothalamic PPII activity, along with high thyrotropin serum concentration. Post-weaning Zn-deficiency (CD) decreased PPII activity only in adenohypophysis and increased thyrotropin circulating levels. Zn-replenishment (DC) normalized PPII activity in both regions and serum thyrotropin concentration. Adenohypophyseal PPII activity decreased and prolactin levels increased in Zn-deficient dams. We concluded that long-term changes in dietary Zn down-regulate PPII activity independently of T3, increasing thyrotropin serum concentration, overall resembling sub-clinical hypothyroidism.

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Section: Discussionsupporting

confidence: 80%

Mediobasal hypothalamic and adenohypophyseal TRH‐degrading enzyme (PPII) is down‐regulated by zinc deficiency

Alvarez-Salas

Alcántara-Alonso

Matamoros-Trejo

et al. 2015

Intl J of Devlp Neuroscience

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“…Recent evidence has suggested that inactivation of TRH in the median eminence by pyroglutamyl peptidase II (PPII), a membrane-bound, highly specific TRH peptidase expressed in the tanycytes (Charli, et al 1998; Heuer, et al 2000), contributes to central regulation of TSH secretion (Sanchez, et al 2009). PPII is also expressed in lactotrophs and somatotrophs in the rat pituitary but not thyrotrophs (Cruz, et al 2008; Heuer, et al 1998) indicating that pituitary PPII may not be involved in TSH regulation. As PPII synthesis is a T3-dependent process, with PPII mRNA being induced in the median eminence within a few hours of exposure to T3 or T4 (Sanchez et al 2009), it suggests that its acute effects to inactivate TRH are localized in this region.…”

Section: Introductionmentioning

confidence: 98%

Thyroxine-induced expression of pyroglutamyl peptidase II and inhibition of TSH release precedes suppression of TRH mRNA and requires type 2 deiodinase

Marsili

Sánchez²,

Singru³

et al. 2011

Journal of Endocrinology

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Suppression of TSH release from the hypothyroid thyrotrophs is one of the most rapid effects of T3 or T4. It is initiated within an hour, and precedes the decrease in TSHβ mRNA inhibition and is blocked by inhibitors of mRNA or protein synthesis. TSH elevation in primary hypothyroidism requires both the loss of feedback inhibition by thyroid hormone in the thyrotrophs and the positive effects of TRH. Another event in this feed back regulation may be the thyroid hormone induction of the TRH-inactivating pyroglutamyl peptidase II (PPII) in the hypothalamic tanycytes. This study compared the chronology of the acute effects of T3 or T4 on TSH suppression, TRH mRNA in the hypothalamic paraventricular nucleus (PVN), and the induction of tanycyte PPII. In wild type mice, T3 or T4 caused a 50% decrease in serum TSH in hypothyroid mice by 5 hours. There was no change in TRH mRNA in PVN over this interval, but there was a significant increase in PPII mRNA in the tanycytes. In mice with genetic inactivation of the type 2 iodothyronine deiodinase, T3 decreased serum TSH and increased PPII mRNA levels, while T4-treatment was ineffective. We conclude that the rapid suppression of TSH in the hypothyroid mouse by T3 occurs prior to a decrease in TRH mRNA though TRH inactivation may be occurring in the median eminence through the rapid induction of tanycyte PPII. The effect of T4, but not T3, requires the type 2 iodothyronine deiodinase.

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“…Interestingly, thyrotropin-releasing hormone degrading enzyme (TRH-DE) is highly expressed in the mouse nucleus incertus (Lein et al, 2007). TRH-DE is known to inactivate TRH (Wilk, 1986), and subsequently plays a role in controlling both TRH-induced TSH release and prolactin release in the anterior pituitary (Cruz et al, 2008;Sanchez et al, 2009). It is possible, therefore, that the nucleus incertus is a target for TRH under certain physiological conditions.…”

Section: Other Modulatory Roles In Reproduction and Metabolism?mentioning

confidence: 99%

Relaxin-3 systems in the brain—The first 10 years

Smith

Ryan

Hosken

et al. 2011

Journal of Chemical Neuroanatomy

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Anterior pituitary pyroglutamyl peptidase II activity controls TRH-induced prolactin release

Cited by 19 publications

References 55 publications

Mediobasal hypothalamic and adenohypophyseal TRH‐degrading enzyme (PPII) is down‐regulated by zinc deficiency

Mediobasal hypothalamic and adenohypophyseal TRH‐degrading enzyme (PPII) is down‐regulated by zinc deficiency

Thyroxine-induced expression of pyroglutamyl peptidase II and inhibition of TSH release precedes suppression of TRH mRNA and requires type 2 deiodinase

Relaxin-3 systems in the brain—The first 10 years

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