scholarly journals Biological intersection of sex, age, and environment in the corticotropin releasing factor (CRF) system and alcohol

2020 ◽  
Vol 170 ◽  
pp. 108045
Author(s):  
Abigail E. Agoglia ◽  
Elizabeth J. Crofton ◽  
Melissa A. Herman
Keyword(s):  
Corticotropin Releasing Factor ◽  
Crf System

scholarly journals Corticotropin-Releasing Factor Inhibits Luteinizing Hormone-Stimulated P450c17 Gene Expression and Androgen Production by Isolated Thecal Cells of Human Ovarian Follicles1

1998 ◽  
Vol 83 (2) ◽  
pp. 448-452
Author(s):  
H. F. Erden ◽  
I. H. Zwain ◽  
H. Asakura ◽  
S. S. C. Yen
Keyword(s):  
Gene Expression ◽  
Granulosa Cells ◽  
Inhibitory Effect ◽  
Corticotropin Releasing Factor ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Messenger Ribonucleic Acid ◽  
Estrogen Production ◽  
Thecal Cells ◽  
Crf System

Recently, we reported that the thecal compartment of the human ovary contains a CRF system replete with gene expression and protein for corticotropin-releasing factor (CRF), CRF-Receptor 1 (CRF-R1), and the blood-derived high affinity CRF-binding protein (CRF-BP). Granulosa cells are devoid of the CRF system. The parallel increases in intensity of CRF, CRF-R1, and 17α-hydroxylase messenger ribonucleic acid (mRNA) and proteins in thecal cells with follicular maturation suggest that the intraovarian CRF system may play an autocrine role regulating androgen biosynthesis, with a downstream effect on estrogen production by granulosa cells. The functionality of the ovarian CRF system may be conditioned by the relative presence of plasma-derived CRF-BP by virtue of its localization of protein, but not transcript in thecal cells and its ability to compete with CRF for the CRF receptor. To further these findings, in the present study we have examined the effect of CRF on LH-stimulated 17α-hydroxylase (P450c17) gene expression and androgen production by isolated thecal cells from human ovarian follicles (11–13 mm). During the 48-h culture, addition of LH (10 ng/mL) to the medium increased by 5- and 6-fold dehydroepiandrosterone and androstenedione production by thecal cells. Remarkably, the LH-stimulated, but not basal, androgen production was inhibited by CRF in a time- and dose-dependent manner. The half-maximal (ID50) effect dose of CRF occurred at 5 × 10−8 mol/L, and at a maximal concentration of 10−6 mol/L, CRF completely inhibited LH-stimulated androgen production. This inhibitory effect of CRF became evident at 12 h (45%), and by 24 h the effect was more pronounced, with a 70% reduction from baseline. As determined by Northern analyses, CRF dose dependently decreased LH-stimulated P450c17 mRNA levels, with a maximal inhibition of 85% P450c17 gene expression at a CRF concentration of 10−6 mol/L. With the addition of 10−6 mol/L of the antagonist α-helical CRF-(9–41), the inhibitory effect of CRF was partially reversed for both P450c17 mRNA (75%) and androgen production (50%), indicating the CRF-R1-mediated event. In conclusion, the present study demonstrated a potent inhibitory effect of CRF on LH-stimulated dehydroepiandrosterone and androstenedione production that appears to be mediated through the reduction of P450c17 gene expression. Thus, the ovarian CRF system may function as autocrine regulators for androgen biosynthesis in the thecal cell compartment to maintain optimal substrate for estrogen biosynthesis by granulosa cells. Further studies to define the role of CRF-BP in the endocrine modulation of the intraovarian CRF system are needed.

The Paraventriculo-Infundibular Corticotropin Releasing Factor (CRF)-System II. Functional Aspects

1985 ◽  
pp. 21-37 ◽  
Author(s):  
István Lengvári ◽  
Magdolna Kovács ◽  
Zsolt Liposits ◽  
Sándor Vigh ◽  
Béla Flerkó
Keyword(s):  
Corticotropin Releasing Factor ◽  
Functional Aspects ◽  
Crf System

Corticotropin-releasing factor (CRF) system localization in human fetal heart

HORMONES ◽  
2016 ◽  
Vol 15 (1) ◽  
pp. 54-64 ◽  
Author(s):  
Efterpi Chouridou ◽  
Maria Lambropoulou ◽  
Maria Koureta ◽  
Christina Zarouchlioti ◽  
Ioanna Balgouranidou ◽  
...  
Keyword(s):  
Fetal Heart ◽  
Corticotropin Releasing Factor ◽  
Human Fetal Heart ◽  
Crf System

scholarly journals Corticotropin-releasing factor (CRF) system localization in human fetal heart

HORMONES ◽  
2016 ◽  
Author(s):  
Efterpi Chouridou ◽  
Maria Lambropoulou ◽  
Maria Koureta ◽  
Christina Zarouchlioti ◽  
Ioanna Balgouranidou ◽  
...  
Keyword(s):  
Fetal Heart ◽  
Corticotropin Releasing Factor ◽  
Human Fetal Heart ◽  
Crf System

Quantitative comparison of mRNA level of corticotropin- releasing factor peptide family in normal kidney and corresponding clear cell renal cell carcinoma specimens.

2015 ◽  
Vol 33 (7_suppl) ◽  
pp. 466-466
Author(s):  
Hossein Tezval ◽  
Axel S. Merseburger ◽  
Markus A. Kuczyk ◽  
Christoph von Klot ◽  
Juergen Serth
Keyword(s):  
Cell Carcinoma ◽  
Clear Cell ◽  
Mrna Level ◽  
Corticotropin Releasing Factor ◽  
Mrna Levels ◽  
Normal Kidney ◽  
Cell Renal Cell Carcinoma ◽  
Inhibition Of Proliferation ◽  
Peptide Family ◽  
Crf System

466 Background: Urocortin (Ucn), a 40 amino acid peptide, belongs to the corticotropin releasing factor (CRF) family and exerts its actions mainly in the periphery through activation of two CRF receptors (CRFRs), CRFR1 and CRFR2 and a binding protein (CRFBP/CRHBP). Both receptors are G-protein coupled and binding of Ucn leads to activation of cAMP-dependent protein kinases via elevation of cAMP levels. Ucn and Urocortin III (UcnIII) are involved in conditions such as regulation of local inflammation, angiogenesis, and inhibition of proliferation. Suppression of neovascularization and inhibition of tumor cell cycling by Urocortins is modulated through CRFRs. Activation of CRFRs by e.g. Ucn inhibits angiogenesis via reduction of vascular endothelial growth factor (VEGF) and suppresses the cell proliferation. Here we characterized the whole CRF family on mRNA levels quantitatively comparing the normal and clear cell carcinoma of the kidney (ccRCC). Methods: In this study we measured the mRNA level of Ucn, UcnIII, CRFR1, CRFR2 and CRHBP in 78 RCC samples and paired histologically normal appearing tissues using quantitative PCR. Statistical analyses were carried out using univariate logistic regression analysis. Results: We found tumour specific down regulation of mRNA expression of UcnIII, CRFR1, CRFR2 and CRHBP in samples of RCCs with clear cell histology compared to paired normal tissues (P<0.01 for all targets). Only Ucn did not show any expression difference between two groups (p=0.17). Conclusions: For the first time we showed the expression profile of the whole CRF peptide family in ccRCC compared to normal kidney on mRNA level. Our data underlines the malfunction of this actually strong protective and anticancer system in renal malignancy and shows the involvement of CRF system in carcinogenesis in kidney. More studies are necessary to find out the detailed roles of the CRF system in renal carcinoma.

The Role of the Glutamatergic System in Posttraumatic Stress Disorder

CNS Spectrums ◽  
2008 ◽  
Vol 13 (7) ◽  
pp. 585-591 ◽  
Author(s):  
Jyotsna Nair ◽  
Sarbjot Singh Ajit
Keyword(s):  
Posttraumatic Stress Disorder ◽  
Anxiety Disorders ◽  
Posttraumatic Stress ◽  
Stress Disorder ◽  
Brain Regions ◽  
Corticotropin Releasing Factor ◽  
Glutamatergic System ◽  
Symptom Complex ◽  
Crf System

ABSTRACTAntiglutamatergic agents, such as lamotrigine, have been used successfully for the treatment of posttraumatic stress disorder (PTSD). They could be potentially acting through the stabilization of the corticotropin-releasing factor (CRF) systems. Glutamate mediates CRF release in various brain regions involved in the pathophysiology of PTSD, antiglutamatergic agents could stabilize the CRF system and, thereby, improve the symptom complex of PTSD (reexperiencing, hyperarousal, and avoidance). The role of glutamate and CRF in PTSD and other anxiety disorders are still being elucidated. However, it is clear that the glutamatergic systems play a role in the pathophysiology of PTSD.

scholarly journals Expression of Genes Encoding Corticotropin-Releasing Factor (CRF), Type 1 CRF Receptor, and CRF-Binding Protein and Localization of the Gene Products in the Human Ovary1

1997 ◽  
Vol 82 (8) ◽  
pp. 2720-2725
Author(s):  
H. Asakura ◽  
I. H. Zwain ◽  
S. S. C. Yen
Keyword(s):  
Granulosa Cells ◽  
Stromal Cells ◽  
Binding Protein ◽  
Corticotropin Releasing Factor ◽  
Human Ovary ◽  
Antral Follicles ◽  
Estrogen Production ◽  
Thecal Cells ◽  
Crf System

Recently, the presence of immunoreactive corticotropin-releasing factor (IrCRF) in the thecal-stromal cells of the human ovary and the ability of CRF to suppress estrogen production by human granulosa cells in vitro have been reported. To understand the functional role of ovarian CRF requires characterization of the human ovarian CRF system, which includes CRF, type 1 CRF receptor (CRF-R1), and the high affinity CRF-binding protein (CRF-BP). Accordingly, we have examined the ovarian CRF system and the cellular distribution of these proteins and their messenger ribonucleic acids (mRNAs) using immunohistochemistry and in situ hybridization, respectively. Normal ovaries from 10 premenopausal women undergoing hysterectomy with ovariectomy were used in the analyses. IrCRF and its mRNA were localized in thecal cells of small antral and mature follicles. A low abundance of IrCRF and mRNA was also detected in stromal cells of both stages of follicles. Expression of the gene encoding CRF was more prominent in mature follicles than in small antral follicles. CRF-R1 mRNA signal was found exclusively in thecal cells of mature follicles and moderately in small antral follicles. Granulosa cells were devoid of CRF and CRF-R1 mRNAs and proteins. The IrCRF-BP, but not its transcript, was detected in thecal cells and lumen of capillary vessels of the thecal/stromal compartment of mature follicles. The absence of CRF-BP gene transcript in human ovarian follicles was confirmed by reverse transcription-PCR, indicating that the IrCRF-BP detected is not derived from the ovarian transcript and suggesting that the presence of IrCRF-BP and luman of capillary vessels in the thecal compartment originates from the peripheral circulation. Thecal cells of mature follicles, relative to those of small antral follicles, exhibited an intensive immunostaining and mRNA signal for 17α-hydroxylase (P450c17) indicative of androgen biosynthesis. We conclude that the thecal compartment of the human ovary contains a CRF system endowed with CRF and CRF-R1 and the blood-derived CRF-BP. Granulosa cells are devoid of the CRF system. The parallel increases in intensity of CRF, CRF-R1, and 17α-hydroxylase proteins and gene expression with follicular maturation suggest that the intraovarian CRF system may play an autocrine role in androgen biosynthesis with a downstream effect on estrogen production by the granulosa cells. The functionality of the ovarian CRF system may be conditioned by the relative presence of circulating CRF-BP by virtue of its ability to compete with CRF for the CRF receptor.

The effects of neonatal stress on brain development: Implications for psychopathology

1999 ◽  
Vol 11 (3) ◽  
pp. 545-565 ◽  
Author(s):  
YOLANDA P. GRAHAM ◽  
CHRISTINE HEIM ◽  
SHERRYL H. GOODMAN ◽  
ANDREW H. MILLER ◽  
CHARLES B. NEMEROFF
Keyword(s):  
Life Stress ◽  
Nonhuman Primates ◽  
Stress Disorder ◽  
Early Life Stress ◽  
Corticotropin Releasing Factor ◽  
Adverse Life Events ◽  
Adverse Experiences ◽  
Increased Sensitivity ◽  
Pituitary Adrenal Axis ◽  
Crf System

Recent studies have focused on the behavioral and neurobiological sequella of exposure to early adverse events. We hypothesize that early adverse experiences result in an increased sensitivity to the effects of stress later in life and render an individual vulnerable to stress-related psychiatric disorders. This vulnerability may be mediated by persistent changes in corticotropin-releasing-factor (CRF)-containing neurons, the hypothalamic–pituitary–adrenal axis, and the sympathetic nervous system. We therefore present an overview of the CRF system and its role as a mediator in the development of the stress response, major depression, and posttraumatic stress disorder. The literature pertaining to behavioral and neurobiological alterations associated with exposure to early adverse life events in rodents, nonhuman primates, and humans is reviewed. We focus on animal models that precipitate depressive and anxiety symptoms while producing neuroendocrine alterations that mimic those seen in adults with those disorders. The literature integrating neurobiological and behavioral consequences of early life stress is also reviewed, focusing primarily on infants born to mothers with depression and on infants who were abused or neglected.

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