Thyrotropin-Releasing Hormone Gene Expression in the Anterior Pituitary. IV. Evidence for Paracrine and Autocrine Regulation

Bruhn, Thomas; Rondeel, J. M. M.; Jackson, Ivor M. D.

doi:10.1210/endo.139.8.6146

Cited by 18 publications

(12 citation statements)

References 48 publications

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“…The subsequent experiments on the effect of dexamethasone on the secretion of ppTRH178-199 may help provide some explanation. We observed a decrease in secretion of ppTRH178-199 in the presence of dexamethasone, consistent with earlier studies of Bruhn et al (1998), who made a similar observation, despite a stimulatory effect of dexamethasone on ppTRH mRNA and precursor protein. If glucocorticoids inhibit secretion of ppTRH178-199, then the removal of glucocorticoids would allow increased secretion of ppTRH178-199, potentially assuming the modulatory role on ACTH secretion of the steroids.…”

Section: Discussionsupporting

confidence: 93%

Prepro-thyrotropin-releasing hormone 178-199 increases sensitivity of AtT-20 cells to dexamethasone

Revskoy

Schwartz²,

Redei

2001

Journal of Endocrinology

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The prepro-thyrotropin-releasing hormone (ppTRH)-derived peptide, ppTRH178-199, has been proposed to inhibit ACTH release at the level of the pituitary and attenuate prolactin and behavioral responses to stress as well. The objective of this study was to elucidate a possible link between the effects of ppTRH178-199 and glucocorticoids on the inhibition of ACTH release in corticotrophs. Compared with mock-transfected cells, AtT-20 cells that were stably transfected with full-length ppTRH cDNA showed significantly increased sensitivity to dexamethasone, as measured by inhibition of ACTH release. In a group of control cells, expressing a mutated form of ppTRH cDNA lacking the ppTRH178-199 region, sensitivity to dexamethasone was not different from mock-transfected controls. Exogenous ppTRH178-199 also increased the inhibitory effect of dexamethasone in wild-type AtT-20 cells. The combined effect of dexamethasone and ppTRH cDNA in cells that express the latter was not due to increased endogenous secretion of ppTRH178-199 in response to dexamethasone, as dexamethasone was independently found to inhibit secretion of ppTRH178-199. Taken together, these data suggest that ppTRH178-199 can interact with the glucocorticoid negative feedback inhibition to regulate ACTH secretion.

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Section: Discussionsupporting

confidence: 93%

Prepro-thyrotropin-releasing hormone 178-199 increases sensitivity of AtT-20 cells to dexamethasone

Revskoy

Schwartz²,

Redei

2001

Journal of Endocrinology

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Section: Discussionmentioning

confidence: 99%

“…Paracrine and autocrine regulation of pituitary TSH and corticotropin (ACTH) by the intrapituitary expression of neuropeptides has been reported in humans and rats (Pagesy et al 1992, Bruhn et al 1998, Giraldi & Cavagnini 1998. TRH mRNA was localized to rat pituitary somatotropes (Bruhn 1994a,b,c) and TRH of pituitary origin can modulate both the secretion of TSH and the biosynthesis of pituitary TRH respectively (Bruhn et al 1998). Similarly, CRF mRNA was localized to the corticotropes in the rat pituitary (Thompson 1987, Giraldi & Cavagnini 1998 and there is evidence for the regulation of ACTH secretion by CRF of pituitary origin (Giraldi & Cavagnini 1998).…”

Section: Discussionmentioning

confidence: 99%

Regulation of pituitary thyrotropin gene expression during Xenopus metamorphosis: negative feedback is functional throughout metamorphosis

Manzon¹,

Denver²

2004

Journal of Endocrinology

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Several hypotheses have been proposed to explain the increase and sustained expression of pituitary thyrotropin (TSH) in the presence of elevated plasma thyroid hormone (TH) concentrations at metamorphic climax in amphibians. It has been proposed that the negative feedback of TH on TSH is inoperative until metamorphic climax, and that it is established at this time by the upregulation of pituitary deiodinase type II (DII); DII converts thyroxine (T 4 ) to 3,5,3 -triiodothyronine (T 3 ). However, earlier investigators, using indirect measures of TSH, reported that TH negative feedback on TSH was functional in premetamorphic tadpoles. In an effort to understand pituitary TSH regulation during amphibian metamorphosis, we analyzed multiple pituitary genes known or hypothesized to be involved in TSH regulation in tadpoles of Xenopus laevis. Tadpole pituitary explant cultures were used to examine direct negative feedback on TSH mRNA expression. Negative feedback is operative in the early prometamorphic tadpole pituitary and both T 3 and T 4 can downregulate TSH mRNA expression throughout metamorphosis. The expression of both DII and TH receptor A mRNAs increased during development and peaked at climax; however, these increases coincided with similar increases in deiodinase type III, which inactivates TH. Moreover, corticotropin-releasing factor (CRF) receptors, CRF binding protein and thyrotropin-releasing hormone receptor type 2 mRNA expression also peaked at climax. Our data suggest that the regulation of TSH is more complex than the timing of DII expression, and likely involves a balance between stimulation of TSH synthesis and secretion by neuropeptides (e.g. CRF) of hypothalamic or pituitary origin, increased pituitary sensitivity to neuropeptides through upregulation of their receptors, and intrapituitary TH levels.

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“…Production of prolactin (PRL) by lactotropes in the anterior pituitary (AP) gland can be regulated by many inhibitory and stimulatory factors released from the hypothalamus and synthesized in the pituitary as well as by the circulating hormones [1, 2, 3, 4, 5]. Among these factors, 17β-estradiol (E 2 ), thyroid hormones, and thyrotropin-releasing hormone (TRH) are known to affect both synthesis and secretion of PRL [1, 5, 6, 7, 8].…”

Section: Introductionmentioning

confidence: 99%

“…Among these factors, 17β-estradiol (E 2 ), thyroid hormones, and thyrotropin-releasing hormone (TRH) are known to affect both synthesis and secretion of PRL [1, 5, 6, 7, 8]. E 2 and triiodothyronine (T 3 ) have also been shown to influence lactotrope responses to PRL inhibitory and stimulatory factors [4, 7, 9].…”

Section: Introductionmentioning

confidence: 99%

Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

Pu¹,

Tan²,

Chen³

et al. 1999

Neuroendocrinology

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Acetylcholine (ACh), synthesized in the pituitary, can act locally to modulate pituitary function. We used rat primary anterior pituitary (AP) cells to investigate how ACh affects pituitary prolactin (PRL) secretion in the presence or absence of known PRL regulators: thyrotropin-releasing hormone (TRH), 17β-estradiol (E₂) and triiodothyronine (T₃). Cultured AP cells were prepared from ovariectomized rats and pretreated with diluent, 0.6 nM E₂, 10 nM T₃, or E₂ plus T₃ for 5 days, then challenged with various doses of ACh or muscarinic receptor agonists (oxotremorine or carbachol) and TRH (100 nM) for 20 min. Significant ACh (10^–5M) suppression of both basal and TRH-induced PRL secretion was not evident in diluent-, E₂- or T₃-pretreated cells, but observed only in cells pretreated with both E₂ and T₃. Moreover, in E₂ plus T₃-pretreated cells, oxotremorine and carbachol, like ACh (10^–7–10^–5M), suppressed both responses in a dose- related manner. Pertussis toxin (PTX; 100 ng/ml) as well as atropine (a muscarinic receptor antagonist; 1 mM) blocked these effects of cholinomimetics. ACh also inhibited both PRL responses elicited by drugs elevating intracellular cAMP (10 µM forskolin) or Ca²⁺ (1 µM Bay K-8644) in a PTX-sensitive manner. ACh inhibition of basal PRL secretion was unaltered by intracellular Ca²⁺ mobilization blockers, TMB-8 (100 µM) and thapsigargin (1 µM), but abrogated by the nitric oxide synthase inhibitor (300 µM L-NAME). ACh inhibition of TRH-induced PRL secretion was accentuated by TMB-8 and alleviated by thapsigargin or L-NAME. In summary, muscarinic inhibition of either basal or TRH-induced PRL secretion was augmented by E₂ and T₃, and involved the PTX-sensitive cAMP/Ca²⁺ pathways. Furthermore, nitric oxide mediated the basal rather than TRH-induced PRL response to ACh, whereas the intracellular Ca²⁺ mobilization concerned the TRH-induced rather than the basal PRL response to ACh. Thus, ACh synthesized in the AP appears to inhibit basal vs. TRH-induced PRL secretion via different mechanisms.

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Thyrotropin-Releasing Hormone Gene Expression in the Anterior Pituitary. IV. Evidence for Paracrine and Autocrine Regulation

Cited by 18 publications

References 48 publications

Prepro-thyrotropin-releasing hormone 178-199 increases sensitivity of AtT-20 cells to dexamethasone

Prepro-thyrotropin-releasing hormone 178-199 increases sensitivity of AtT-20 cells to dexamethasone

Regulation of pituitary thyrotropin gene expression during Xenopus metamorphosis: negative feedback is functional throughout metamorphosis

Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

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