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Fraser Aird - One of the best experts on this subject based on the ideXlab platform.
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a novel endogenous Corticotropin Release inhibiting factor
Annals of the New York Academy of Sciences, 1998Co-Authors: Eva E Redei, Peter A Rittenhouse, Sergei Revskoy, Robert F Mcgivern, Fraser AirdAbstract:ACTH is the major regulator of the body's adaptive response to stress and the physiological stimulus for glucocorticoid secretion. A hypothalamic Corticotropin Release inhibiting factor (CRIF) that inhibits ACTH synthesis and secretion has long been postulated but was not characterized until recently. We have recently identified a 22 amino acid peptide, prepro-thyrotropin releasing hormone (TRH) 178-199 that inhibits basal and stimulated ACTH synthesis and secretion in vitro and stress-induced ACTH secretion in vivo. Prepro-TRH 178-199 is abundant in several brain regions, including the external zone of the median eminence, where its concentration changes in response to stress. We propose that this peptide is a physiological regulator of ACTH production: an endogenous CRIF. Because prepro-TRH 178-199 is encoded within the same precursor as TRH, its expression is likely to be negatively regulated by thyroid hormones leading to changes in endogenous glucocorticoid levels. Streptococcal cell wall (SCW)-induced inflammation, a model of rheumatoid arthritis (RA), was alleviated after long-term thyroxine treatment. Inversely, a hypothyroid milieu led to decreased basal hypothalamic-pituitary-adrenal activity, but increased expression of IL-1 beta and MIP-1 alpha, specific markers for RA in humans. These results suggest that this putative CRIF may be an important component in the development of RA and that regulation of prepro TRH may be highly relevant to the development of other autoimmune diseases that are also exacerbated by low endogenous glucocorticoid levels.
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Corticotropin Release inhibiting factor is preprothyrotropin releasing hormone 178 199
Endocrinology, 1995Co-Authors: Eva E Redei, Harold Hilderbrand, Fraser AirdAbstract:ACTH is the major regulator of the body's adaptive response to stress and the physiological stimulus for glucocorticoid secretion. In addition to the known negative feedback regulation of ACTH by glucocorticoids, a hypothalamic Corticotropin Release-inhibiting factor (CRIF) that inhibits ACTH synthesis and secretion has been postulated, but not identified. We previously reported that transfection of prepro-TRH complementary DNA into the mouse anterior pituitary tumor cell line AtT-20 results in inhibition of basal and Corticotropin-releasing hormone (CRH)-stimulated ACTH synthesis and secretion, suggesting that one or more of the cryptic peptides encoded within the prepro-TRH precursor has CRIF activity. To narrow the choice of peptides responsible for CRIF activity, we first deleted specific sequences within the prepro-TRH complementary DNA and transfected these constructs into AtT-20 cells. Deletion of sequences encoding amino acids 119-229 resulted in the loss of CRIF activity. Of the peptides encoded ...
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Corticotropin Release inhibiting factor is encoded within prepro trh
Endocrinology, 1995Co-Authors: Eva E Redei, Harold Hilderbrand, Fraser AirdAbstract:Corticotropin synthesis and secretion is under negative feedback regulation by glucocorticoids. In addition a hypothalamic factor inhibiting ACTH synthesis and secretion, named Corticotropin Release inhibiting factor (CRIF), has been postulated but not identified. Here we report that transient transfection of a rat prepro-TRH cDNA into the mouse anterior pituitary tumor cell line AtT-20 inhibits the synthesis and secretion of both basal and CRH-stimulated ACTH. Thus, CRIF appears to be encoded by the same precursor as TRH, suggesting a coordinated regulation of pituitary-adrenal and pituitary-thyroid functions.
Eva E Redei - One of the best experts on this subject based on the ideXlab platform.
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the Corticotropin Release inhibitory factor hypothesis a review of the evidence for the existence of inhibitory as well as stimulatory hypophysiotropic regulation of adrenoCorticotropin secretion and biosynthesis
Endocrine Reviews, 1999Co-Authors: Dennis Engler, Eva E Redei, Ismail KolaAbstract:I. Introduction II. Hypothalamic Stimulation of ACTH Release and Biosynthesis A. Corticotropin-releasing factor (CRF) B. Arginine vasopressin (AVP) C. The hypothalamic CRF and AVP neurons and their connections D. Studies of the secretion of CRF and AVP into the hypophysial-portal circulation E. Studies of the neural regulation of CRF and AVP secretion and biosynthesis III. Hypothalamic Inhibition of ACTH Release and Biosynthesis A. Historic studies B. Effect of hypothalamo-pituitary disconnection in adult and fetal sheep C. Effects of the opiate alkaloids and opioid peptides on the HPA axis D. The role of the posterior pituitary in the regulation of corticotropic function E. Hypothalamic ACTH Release-inhibitory activity F. Definition of Corticotropin Release inhibitory factor (CRIF) IV. CRIF: A Consideration of Possible Candidates A. Somatostatin (SST) B. Dopamine C. Atrial natriuretic peptide (ANP) D. Prepro-TRH-(178–199) E. Other substances V. Future Directions
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a novel endogenous Corticotropin Release inhibiting factor
Annals of the New York Academy of Sciences, 1998Co-Authors: Eva E Redei, Peter A Rittenhouse, Sergei Revskoy, Robert F Mcgivern, Fraser AirdAbstract:ACTH is the major regulator of the body's adaptive response to stress and the physiological stimulus for glucocorticoid secretion. A hypothalamic Corticotropin Release inhibiting factor (CRIF) that inhibits ACTH synthesis and secretion has long been postulated but was not characterized until recently. We have recently identified a 22 amino acid peptide, prepro-thyrotropin releasing hormone (TRH) 178-199 that inhibits basal and stimulated ACTH synthesis and secretion in vitro and stress-induced ACTH secretion in vivo. Prepro-TRH 178-199 is abundant in several brain regions, including the external zone of the median eminence, where its concentration changes in response to stress. We propose that this peptide is a physiological regulator of ACTH production: an endogenous CRIF. Because prepro-TRH 178-199 is encoded within the same precursor as TRH, its expression is likely to be negatively regulated by thyroid hormones leading to changes in endogenous glucocorticoid levels. Streptococcal cell wall (SCW)-induced inflammation, a model of rheumatoid arthritis (RA), was alleviated after long-term thyroxine treatment. Inversely, a hypothyroid milieu led to decreased basal hypothalamic-pituitary-adrenal activity, but increased expression of IL-1 beta and MIP-1 alpha, specific markers for RA in humans. These results suggest that this putative CRIF may be an important component in the development of RA and that regulation of prepro TRH may be highly relevant to the development of other autoimmune diseases that are also exacerbated by low endogenous glucocorticoid levels.
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Corticotropin Release inhibiting factor is preprothyrotropin releasing hormone 178 199
Endocrinology, 1995Co-Authors: Eva E Redei, Harold Hilderbrand, Fraser AirdAbstract:ACTH is the major regulator of the body's adaptive response to stress and the physiological stimulus for glucocorticoid secretion. In addition to the known negative feedback regulation of ACTH by glucocorticoids, a hypothalamic Corticotropin Release-inhibiting factor (CRIF) that inhibits ACTH synthesis and secretion has been postulated, but not identified. We previously reported that transfection of prepro-TRH complementary DNA into the mouse anterior pituitary tumor cell line AtT-20 results in inhibition of basal and Corticotropin-releasing hormone (CRH)-stimulated ACTH synthesis and secretion, suggesting that one or more of the cryptic peptides encoded within the prepro-TRH precursor has CRIF activity. To narrow the choice of peptides responsible for CRIF activity, we first deleted specific sequences within the prepro-TRH complementary DNA and transfected these constructs into AtT-20 cells. Deletion of sequences encoding amino acids 119-229 resulted in the loss of CRIF activity. Of the peptides encoded ...
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Corticotropin Release inhibiting factor is encoded within prepro trh
Endocrinology, 1995Co-Authors: Eva E Redei, Harold Hilderbrand, Fraser AirdAbstract:Corticotropin synthesis and secretion is under negative feedback regulation by glucocorticoids. In addition a hypothalamic factor inhibiting ACTH synthesis and secretion, named Corticotropin Release inhibiting factor (CRIF), has been postulated but not identified. Here we report that transient transfection of a rat prepro-TRH cDNA into the mouse anterior pituitary tumor cell line AtT-20 inhibits the synthesis and secretion of both basal and CRH-stimulated ACTH. Thus, CRIF appears to be encoded by the same precursor as TRH, suggesting a coordinated regulation of pituitary-adrenal and pituitary-thyroid functions.
Salvatore Maria Corsello - One of the best experts on this subject based on the ideXlab platform.
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Treatment with Synthetic Glucocorticoids and the Hypothalamus-Pituitary-Adrenal Axis
International journal of molecular sciences, 2017Co-Authors: Rosa Maria Paragliola, Giampaolo Papi, Alfredo Pontecorvi, Salvatore Maria CorselloAbstract:Chronic glucocorticoid (GC) treatment represents a widely-prescribed therapy for several diseases in consideration of both anti-inflammatory and immunosuppressive activity but, if used at high doses for prolonged periods, it can determine the systemic effects characteristic of Cushing’s syndrome. In addition to signs and symptoms of hypercortisolism, patients on chronic GC therapy are at risk to develop tertiary adrenal insufficiency after the reduction or the withdrawal of corticosteroids or during acute stress. This effect is mediated by the negative feedback loop on the hypothalamus-pituitary-adrenal (HPA) axis, which mainly involves Corticotropin-Release hormone (CRH), which represents the most important driver of adrenocorticotropic hormone (ACTH) Release. In fact, after withdrawal of chronic GC treatment, reactivation of CRH secretion is a necessary prerequisite for the recovery of the HPA axis. In addition to the well-known factors which regulate the degree of inhibition of the HPA during synthetic GC therapy (type of compound, method of administration, cumulative dose, duration of the treatment, concomitant drugs which can increase the bioavailability of GCs), there is a considerable variation in individual physiology, probably related to different genetic profiles which regulate GC receptor activity. This may represent an interesting basis for possible future research fields.
Yuxiang Zhang - One of the best experts on this subject based on the ideXlab platform.
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the relationship of ultrastructure and function of hypothalamus pituitary adrenal axis in early stage of sepsis in rats
Chinese critical care medicine, 2011Co-Authors: Yuxiang ZhangAbstract:Objective To observe the changes in ultrastructure and function of hypothalamicpituitary-adrenal axis (HPAA), and to approach the relationship between them in early stage of sepsis in rats. Methods Thirty male Sprague-Dawley (SD) rats were randomly divided into normal control group,sham group, sepsis group. The sepsis model was reproduced by cecal ligation and puncture (CLP). The rats were sacrificed after collection of blood at 6 hours after CLP, and the levels of adrenocorticotropic hormone (ACTH) and corticosterone (CORT) in the plasma, and the Corticotropin Release hormone (CRH) in the tissue of hypothalamus were detected. The histopathological changes in HPAA were observed with transmission electron microscopy. Results The levels of ACTH and CORT in plasma, and the CRH in hypothalamus tissue of sepsis group were increased in the early stage of sepsis compared with the normal control group or sham group [ACTH (pmol/L): 5. 78 ± 0. 36 vs. 1.94 ±0.31, 2. 51 ± 0.10; CORT (nmol/L), 88.48±4.47 vs. 22.02±1.62, 34.20±2.51; CRH (μg/L): 101. 92±6. 61 vs. 61.65±6.05,66. 65±4. 03, P＜0. 05 or P＜0. 01]. The changes in ultrastructure of the hypothalamus, pituitary and adrenal were also found. In sepsis group, the ultrastructure of hypothalamus was as follows. Rough endoplasmic reticulum expansion and degranulation of rough endoplasmic reticulum, and swelling of Golgi complex were found. A large number of endocrine granules could be seen in ATCH cells in the pituitary with depletion of adrenal lipid droplets. Conclusion In septic rats, the HPAA was excessively activated, and ACTH and CORT in plasma, and CRH in hypothalamus were significantly increased in early stage of sepsis.The changes in ultrastructure of HPAA were obvious, and the change in function was closely related to the ultrastructural changes. Key words: Sepsis; Cecal ligation and puncture; Hypothalamic-pituitary-adrenal axis; Trans-mission electron microscopy
Jonathan R Seckl - One of the best experts on this subject based on the ideXlab platform.
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atriopeptin an endogenous Corticotropin Release inhibiting hormone
Endocrinology, 1992Co-Authors: F Antoni, E F M Hunter, P J Lowry, June Noble, Jonathan R SecklAbstract:Activation of the hypothalamic-pituitary-adrenocortical axis is a major component of the body's response to stress. Current theories on the pathophysiology of disorders associated with hyperfunction of the axis, such as depression and Cushing's stress, are based on the concept that anterior pituitary adrenoCorticotropin (ACTH) secretion is stimulated by hypothalamic Corticotropin-releasing hormones and inhibited by adrenal corticosteroids. Hypothalamic inhibitory control of pituitary ACTH secretion has been also postulated, but has not gained general acceptance because of the lack of definitive evidence for a Corticotropin-Release inhibiting hormone. It is shown here that in conscious rats stress-induced secretion of ACTH and corticosterone is markedly enhanced by the immunoneutralisation of atriopeptin. Therefore, we propose that atriopeptin is a physiologically relevant Corticotropin-Release inhibiting hormone.
