Corticotropin-releasing hormone is produced by rat corticotropes and modulates ACTH secretion in a paracrine/autocrine fashion.

Giraldi, Francesco; Cavagnini, Francesco

doi:10.1172/jci443

Cited by 32 publications

(22 citation statements)

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“…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).…”

Section: Discussionmentioning

confidence: 99%

“…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%

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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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Section: Discussionmentioning

confidence: 99%

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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“…Thus, the source of ACTH responded to DDAVP before the surgery was considered to be derived from non-neoplastic portion of the pituitary gland. There have been some reports which show that CRH and Ucn1 are produced in pituitary gland and may regulate ACTH secretion in a paracrine/autocrine fashion [11,21,22]. Therefore, we postulated that paracrine effects by the adenoma affected secretion of ACTH from normal pituitary gland in this case.…”

Section: Immunohistochemistrymentioning

confidence: 65%

“…NeuroD1/β1 and Pit-1 are the transcription factors implicated in the development of individual pituitary cell types to a corticotroph and somatotroph stem cell, respectively [2]. CRF is produced by rat corticotropes [22] and human pituitary corticotroph adenoma [23], and Ucn1 is produced by GH producing pituitary cells [11]. The transcriptional factor, Brn-2, plays an important role in the development of CRF neurons in the hypothalamus [25].…”

Section: Immunohistochemistrymentioning

confidence: 99%

ACTH response to desmopressin in a patient with acromegaly; Expression of corticotropin-releasing factor, urocortins and vasopressin V1b receptor in GH-producing pituitary adenoma

Arihara¹,

Sakurai²,

Osaki³

et al. 2011

Endocr J

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“…In addition to urocortin, the anterior pituitary has recently been shown to synthesize a wide variety of peptides conventionally considered to be hypothalamic-releasing factors, including thyrotropin-releasing hormone, gonadotropin-releasing hormone (29), growth hormone-releasing hormone, somatostatin (19), and CRH (13). In rats, dispersed anterior pituitary cells synthesize and secrete CRH, and incubation of these cells with an antibody directed against CRH significantly decreased ACTH output by the corticotrophs (13).…”

Section: Discussionmentioning

confidence: 99%

Urocortin: a mechanism for the sustained activation of the HPA axis in the late-gestation ovine fetus?

Holloway

Howe

Chan

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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We hypothesized that urocortin might be produced in the pituitary of the late-gestation ovine fetus in a manner that could contribute to the regulation of ACTH output. We used in situ hybridization and immunohistochemistry to identify urocortin mRNA and protein in late-gestation fetal pituitary tissue. Levels of urocortin mRNA rose during late gestation and were associated temporally with rising concentrations of pituitary proopiomelanocortin (POMC) mRNA. Urocortin was localized both to cells expressing ACTH and to non-ACTH cells by use of dual immunofluorescence histochemistry. Transfection of pituitary cultures with urocortin antisense probe reduced ACTH output, whereas added urocortin stimulated ACTH output from cultured pituitary cells. Cortisol infusion for 96 h in chronically catheterized late-gestation fetal sheep significantly stimulated levels of pituitary urocortin mRNA. We conclude that urocortin is expressed in the ovine fetal pituitary and localizes with, and can stimulate output of, ACTH. Regulation of urocortin by cortisol suggests a mechanism to override negative feedback and sustain feedforward of fetal hypothalamic-pituitary-adrenal function, leading to birth. urocortin; adrenocorticotropic hormone; parturition; hypothalamic-pituitary-adrenal axis MATURATION AND ACTIVATION of the fetal hypothalamicpituitary-adrenal (HPA) axis provide the stimulus for the initiation of parturition in sheep. Plasma cortisol concentrations in the fetal lamb increase during late gestation in association with a concomitant rise in fetal plasma adrenocorticotropic hormone (ACTH) (26) and contribute to parturition onset. Chan et al. (9) have suggested that, in the fetal sheep, stimulation of ACTH output by hypothalamic corticotropin-releasing factor (CRF) is a primary factor in the onset of parturition. However, at term, fetal sheep that have undergone hypothalamo-pituitary disconnection have basal plasma ACTH concentrations that are not different from those of the intact control sheep (5, 11). These data suggest that the late-gestational rise in ACTH output may not be solely regulated by hypothalamic input.It has been suggested that hormones secreted within the pituitary may function to regulate hormone secretion from other pituitary cells in a paracrine manner (29,31,34). One such candidate for paracrine regulation of ACTH secretion is urocortin. Urocortin is a member of the CRF peptide family and shows a 45% sequence identity to CRF (32). In the rat, urocortin has been shown to stimulate increases in plasma ACTH (1) and ACTH output from cultured pituitary cells (1, 28) with similar or greater potency than CRF. Recently, it has been reported that the pituitary is the site of the highest immunoreactive urocortin concentrations in both the rat and the human (17, 27). Ovine urocortin has recently been cloned and localized in the brain of the sheep, but there is no information regarding the localization of urocortin in the ovine pituitary or concerning the actions of urocortin on ACTH release in the late-gestational fe...

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Corticotropin-releasing hormone is produced by rat corticotropes and modulates ACTH secretion in a paracrine/autocrine fashion.

Cited by 32 publications

References 50 publications

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

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

ACTH response to desmopressin in a patient with acromegaly; Expression of corticotropin-releasing factor, urocortins and vasopressin V1b receptor in GH-producing pituitary adenoma

Urocortin: a mechanism for the sustained activation of the HPA axis in the late-gestation ovine fetus?

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