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[PMID]:29346425
[Au] Autor:Hooper A; Fuller PM; Maguire J
[Ad] Endereço:Tufts University School of Medicine, Department of Neuroscience, Boston, Massachusetts.
[Ti] Título:Hippocampal corticotropin-releasing hormone neurons support recognition memory and modulate hippocampal excitability.
[So] Source:PLoS One;13(1):e0191363, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Corticotropin-releasing hormone (CRH) signaling in the hippocampus has been established to be important for mediating the effects of stress on learning and memory. Given our laboratory's recent characterization of a subset of hippocampal CRH neurons as a novel class of GABAergic interneurons, we hypothesized that these local GABAergic hippocampal CRH neurons may influence hippocampal function. Here we applied an array of molecular tools to selectively label and manipulate hippocampal CRH neurons in mice, in order to assess this interneuron population's impact on hippocampus-dependent behaviors and hippocampal network excitability. Genetically-targeted ablation of hippocampal CRH neurons in vivo impaired object recognition memory and substantially enhanced the severity of kainic acid-induced seizures. Conversely, selective activation of CRH neurons in vitro suppressed the excitability of the mossy fiber-CA3 pathway. Additional experiments are needed to reconcile the functions of GABA and CRH signaling of hippocampal CRH neurons on hippocampal function. However, our results indicate that this interneuron population plays an important role in maintaining adaptive network excitability, and provide a specific circuit-level mechanism for this role.
[Mh] Termos MeSH primário: Região CA3 Hipocampal/metabolismo
Hormônio Liberador da Corticotropina/metabolismo
Neurônios GABAérgicos/metabolismo
Memória
[Mh] Termos MeSH secundário: Animais
Região CA3 Hipocampal/citologia
Eletroencefalografia
Locomoção
Camundongos
Camundongos Transgênicos
Técnicas de Patch-Clamp
Transdução de Sinais
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; VALIDATION STUDIES
[Nm] Nome de substância:
56-12-2 (gamma-Aminobutyric Acid); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191363


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[PMID]:29080675
[Au] Autor:Chen L; Li S; Cai J; Wei TJ; Liu LY; Zhao HY; Liu BH; Jing HB; Jin ZR; Liu M; Wan Y; Xing GG
[Ad] Endereço:Neuroscience Research Institute, Peking University and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China. Electronic address: chenlin2005cn@163.com.
[Ti] Título:Activation of CRF/CRFR1 signaling in the basolateral nucleus of the amygdala contributes to chronic forced swim-induced depressive-like behaviors in rats.
[So] Source:Behav Brain Res;338:134-142, 2018 Feb 15.
[Is] ISSN:1872-7549
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The basolateral nucleus of the amygdala (BLA) plays a key role in processing stressful events and affective disorders. Previously we have documented that exposure of chronic forced swim (FS) to rats produces a depressive-like behavior and that sensitization of BLA neurons is involved in this process. In the present study, we demonstrated that chronic FS stress (CFSS) could activate corticotropin-releasing factor (CRF)/CRF receptor type 1 (CRFR1) signaling in the BLA, and blockade of CRF/CRFR1 signaling by intra-BLA injection of NBI27914 (NBI), a selective CRFR1 antagonist, could prevent the CFSS-induced depressive-like behaviors in rats, indicating that activation of CRF/CRFR1 signaling in the BLA is required for CFSS-induced depression. Furthermore, we discovered that exposure of chronic FS to rats could reinforce long-term potentiation (LTP) at the external capsule (EC)-BLA synapse and increase BLA neuronal excitability, and that all these alterations were inhibited by CRFR1 antagonist NBI. Moreover, we found that application of exogenous CRF also may facilitate LTP at the EC-BLA synapse and sensitize BLA neuronal excitability in normal rats via the activation of CRFR1. We conclude that activation of CRF/CRFR1 signaling in the BLA contributes to chronic FS-induced depressive-like behaviors in rats through potentiating synaptic efficiency at the EC-BLA pathway and sensitizing BLA neuronal excitability.
[Mh] Termos MeSH primário: Complexo Nuclear Basolateral da Amígdala/metabolismo
Comportamento Animal/fisiologia
Hormônio Liberador da Corticotropina/metabolismo
Depressão/metabolismo
Receptores de Hormônio Liberador da Corticotropina/antagonistas & inibidores
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Compostos de Anilina/farmacologia
Animais
Complexo Nuclear Basolateral da Amígdala/efeitos dos fármacos
Comportamento Animal/efeitos dos fármacos
Masculino
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Pirimidinas/farmacologia
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/efeitos dos fármacos
Estresse Psicológico/metabolismo
Natação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-methyl-4-(N-propyl-N-cycloproanemethylamino)-5-chloro-6-(2,4,6-trichloranilino)pyrimidine); 0 (Aniline Compounds); 0 (CRF receptor type 1); 0 (Pyrimidines); 0 (Receptors, Corticotropin-Releasing Hormone); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171030
[St] Status:MEDLINE


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[PMID]:27777046
[Au] Autor:Endsin MJ; Michalec O; Manzon LA; Lovejoy DA; Manzon RG
[Ad] Endereço:Department of Biology, University of Regina, Regina, Saskatchewan, Canada.
[Ti] Título:CRH peptide evolution occurred in three phases: Evidence from characterizing sea lamprey CRH system members.
[So] Source:Gen Comp Endocrinol;240:162-173, 2017 01 01.
[Is] ISSN:1095-6840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The corticotropin releasing hormone (CRH) system, which includes the CRH family of peptides, their receptors (CRHRs) and a binding protein (CRHBP), has been strongly conserved throughout vertebrate evolution. The identification of invertebrate homologues suggests this system evolved over 500 million years ago. However, the early vertebrate evolution of the CRH system is not understood. Current theory indicates that agnathans (hagfishes and lampreys) are monophyletic with a conservative evolution over the past 500million years and occupy a position at the root of vertebrate phylogeny. We isolated the cDNAs for three CRH family members, two CRHRs and a CRHBP from the sea lamprey, Petromyzon marinus. Two of the CRH peptides are related to the CRH/urotensin-1 (UI) lineage, whereas the other is a urocortin (Ucn) 3 orthologue. The predicted amino acid identity of CRH and UI is 61% but they possess distinct motifs indicative of each peptide, suggesting an early divergence of the two genes. Based on our findings we propose the CRH peptides evolved in at least 3 distinct phases. The first occurring prior to the agnathans gave rise to the CRH/UI-like and Ucn2/3-like paralogous lineages. The second was a partial sub-genomic duplication of the ancestral CRH/UI-like gene, but not the Ucn2/3-like gene, giving rise to the CRH and UI (Ucn) lineages. The third event which resulted in the appearance of Ucn2 and Ucn3 must have occurred after the evolution of the cartilaginous fishes. Interestingly, unlike other vertebrate CRHRs, we were unable to classify our two P. marinus receptors (designated CRHRα and CRHRß) as either type 1 or type 2, indicating that this split evolved later in vertebrate evolution. A single CRHBP gene was found suggesting that either this gene has not been affected by the vertebrate genome duplications or there have been a series of paralogous gene deletions. This study suggests that P. marinus possess a functional CRH system that differs from that of the gnathostomes and may represent a model for the earliest functioning CRH system in vertebrates.
[Mh] Termos MeSH primário: Hormônio Liberador da Corticotropina/genética
Evolução Molecular
Petromyzon/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Análise de Variância
Animais
Hormônio Liberador da Corticotropina/química
DNA Complementar/genética
Genoma
Especificidade de Órgãos/genética
Filogenia
Ligação Proteica
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Alinhamento de Sequência
Análise de Sequência de DNA
Estresse Fisiológico/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (RNA, Messenger); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180124
[Lr] Data última revisão:
180124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:29179184
[Au] Autor:Yue H; Bin L; Chaoying C; Meng Z; Meng L; Xi W
[Ti] Título:Potential Regulatory Effects of Corticotropin-Releasing Factor on Tight Junction-Related Intestinal Epithelial Permeability are Partially Mediated by CK8 Upregulation.
[So] Source:Cell Physiol Biochem;44(3):1161-1173, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Intestinal permeability and stress have been implicated in the pathophysiology of irritable bowel syndrome (IBS). Cytokeratin 8 (CK8), for the first time, has been shown to mediate corticotropin-releasing factor (CRF)-induced changes in intestinal permeability in animal models of IBS. In this study, we investigated the regulatory effects of CRF on the permeability of human intestinal epithelial cells through the CK8-mediated tight junction. METHODS: The expression levels of corticotropin-releasing factor receptor 1 (CRFR1) and corticotropin-releasing factor receptor 2 (CRFR2) on the HT29 cell surface were determined by immunofluorescence, RT-PCR, and Western blotting. After treatment with 100 nM CRF for 72 h, the translocation of FITC-labelled dextran was measured in a transwell chamber; the structural changes of tight junctions were observed under transmission electron microscopy; the expression levels of CK8, F-actin and tight junction proteins ZO-1, claudin-1, and occludin were detected by immunoblotting and immunofluorescence. The activity of RhoA was detected by immunoprecipitation. Furthermore, the effects of CRF on intestinal epithelial permeability were examined in CK8-silenced HT29 cells, which were constructed by shRNA interference. RESULTS: CRF treatment increased FITC-labelled dextran permeability, caused the opening of tight junctions, induced increased fluorescence intensity of CK8 and decreased the intensities of ZO-1, claudin-1, and occludin, together with structural disruption. The expression levels of F-actin, occludin, claudin-1, and ZO-1 were downregulated. RhoA activity peaked at 30 min after CRF treatment. CRF-induced increased permeability, and downregulation of claudin-1 and occludin were not blocked by CK8 silencing. Nevertheless, CK8 silencing blocked the effects of CRF regarding the decrease in the expression levels of F-action and ZO-1 and increase in RhoA activity. CONCLUSION: CRF may increase intestinal epithelial permeability by upregulating CK8 expression, activating the RhoA signalling pathway, promoting intestinal epithelial actin remodelling, and decreasing the expression of the tight junction protein ZO-1. Other CK8-independent pathways may be involved in the downregulation of claudin-1 and occludin, which might also contribute to increased intestinal epithelial permeability.
[Mh] Termos MeSH primário: Hormônio Liberador da Corticotropina/farmacologia
Queratina-8/metabolismo
Permeabilidade/efeitos dos fármacos
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Junções Íntimas/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Actinas/metabolismo
Claudina-1/metabolismo
Células HT29
Seres Humanos
Mucosa Intestinal/citologia
Mucosa Intestinal/metabolismo
Queratina-8/antagonistas & inibidores
Queratina-8/genética
Microscopia Eletrônica
Microscopia de Fluorescência
Ocludina/metabolismo
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Receptores de Hormônio Liberador da Corticotropina/genética
Junções Íntimas/metabolismo
Junções Íntimas/ultraestrutura
Proteína da Zônula de Oclusão-1/metabolismo
Proteína rhoA de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (CRF receptor type 1); 0 (CRF receptor type 2); 0 (Claudin-1); 0 (Keratin-8); 0 (Occludin); 0 (RNA, Small Interfering); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (Zonula Occludens-1 Protein); 9015-71-8 (Corticotropin-Releasing Hormone); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485420


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[PMID]:28743461
[Au] Autor:Liu XH; Wang ZJ; Jin L; Huang J; Pu DY; Wang DS; Zhang YG
[Ad] Endereço:Key Laboratory of Freshwater Fish Reproduction and Development (Ministry of Education), Key Laboratory of Aquatic Science of Chongqing, Southwest University School of Life Sciences, Chongqing 400715, China.
[Ti] Título:Effects of subchronic exposure to waterborne cadmium on H-P-I axis hormones and related genes in rare minnows (Gobiocypris rarus).
[So] Source:Comp Biochem Physiol C Toxicol Pharmacol;202:1-11, 2017 Nov.
[Is] ISSN:1532-0456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The H (hypothalamic)-P (pituitary)-I (interrenal) axis is critical in the stress response and other activities of fish. To further investigate cadmium (Cd) toxicity on the H-P-I axis and to identify its potential regulatory genes in fish, the adult female rare minnows (Gobiocypris rarus) were exposed to subchronic (5weeks) levels of waterborne Cd in the present study. This kind of treatment caused dose-dependent decline in fish growth, with significance in the high dose group (100µg/L). Correspondingly, low dose (5-50µg/L) waterborne Cd disrupted the endocrine system of H-P-I axis just at the secretion level, while high dose Cd disrupted both the secretion and synthesis of cortisol and its downstream signals in rare minnows, revealed by the significantly upregulation and positive correlation of corticosteroidogenic genes including MC2R, StAR, CYP11A1, and CYP11B1 in the kidney (including the interrenal tissue) (P<0.05), and the significant alteration of Glcci1, Hsp90AA and Hsp90AB in the hepatopancreas, gill and intestine as well (P<0.05). The expression of Glcci1 was significantly decreased in hepatopancreas, gill and intestine of tested fish following treatment, and its positive correlation with GR (Glucocorticoid receptor) suggested its potential regulation on the cortisol and/or H-P-I axis in fish. The expression of FKBP5 in the intestine was positively and significantly correlated with that of Hsp90AA (P<0.05), and the Hsp90AB transcript in the hepatopancreas was positively correlated with that of Hsp90AA (P<0.05), which indicated that Hsp90AA and Hsp90AB were more likely to serve as cofactors of GR and FKBP5 in response to Cd exposure.
[Mh] Termos MeSH primário: Cloreto de Cádmio/toxicidade
Cyprinidae/fisiologia
Sistema Hipotálamo-Hipofisário/efeitos dos fármacos
Glândula Inter-Renal/efeitos dos fármacos
[Mh] Termos MeSH secundário: Hormônio Adrenocorticotrópico/genética
Hormônio Adrenocorticotrópico/metabolismo
Animais
Cloreto de Cádmio/administração & dosagem
Hormônio Liberador da Corticotropina/genética
Hormônio Liberador da Corticotropina/metabolismo
Esquema de Medicação
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Hidrocortisona/genética
Hidrocortisona/metabolismo
Sistema Hipotálamo-Hipofisário/fisiologia
Glândula Inter-Renal/fisiologia
Hormônios Estimuladores de Melanócitos/genética
Hormônios Estimuladores de Melanócitos/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Proteínas de Ligação a Tacrolimo/genética
Proteínas de Ligação a Tacrolimo/metabolismo
Poluentes Químicos da Água/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Water Pollutants, Chemical); 9002-60-2 (Adrenocorticotropic Hormone); 9002-79-3 (Melanocyte-Stimulating Hormones); 9015-71-8 (Corticotropin-Releasing Hormone); EC 5.2.1.- (Tacrolimus Binding Proteins); J6K4F9V3BA (Cadmium Chloride); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180109
[Lr] Data última revisão:
180109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE


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[PMID]:28929494
[Au] Autor:Pothoulakis C; Torre-Rojas M; Duran-Padilla MA; Gevorkian J; Zoras O; Chrysos E; Chalkiadakis G; Baritaki S
[Ad] Endereço:IBD Center, Division of Digestive Diseases, David Geffen School of Medicine at UCLA, Los Angeles, CA.
[Ti] Título:CRHR2/Ucn2 signaling is a novel regulator of miR-7/YY1/Fas circuitry contributing to reversal of colorectal cancer cell resistance to Fas-mediated apoptosis.
[So] Source:Int J Cancer;142(2):334-346, 2018 Jan 15.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer (CRC) responds poorly to immuno-mediated cytotoxicity. Underexpression of corticotropin-releasing-hormone-receptor-2 (CRHR2) in CRC, promotes tumor survival, growth and Epithelial to Mesenchymal Transition (EMT), in vitro and in vivo. We explored the role of CRHR2 downregulation in CRC cell resistance to Fas/FasL-mediated apoptosis and the underlying molecular mechanism. CRC cell sensitivity to CH11-induced apoptosis was compared between Urocortin-2 (Ucn2)-stimulated parental and CRHR2-overexpressing CRC cell lines and targets of CRHR2/Ucn2 signaling were identified through in vitro and ex vivo analyses. Induced CRHR2/Ucn2 signaling in SW620 and DLD1 cells increased specifically their sensitivity to CH11-mediated apoptosis, via Fas mRNA and protein upregulation. CRC compared to control tissues had reduced Fas expression that was associated with lost CRHR2 mRNA, poor tumor differentiation and high risk for distant metastasis. YY1 silencing increased Fas promoter activity in SW620 and re-sensitized them to CH11-apoptosis, thus suggesting YY1 as a putative transcriptional repressor of Fas in CRC. An inverse correlation between Fas and YY1 expression was confirmed in CRC tissue arrays, while elevated YY1 mRNA was clinically relevant with advanced CRC grade and higher risk for distant metastasis. CRHR2/Ucn2 signaling downregulated specifically YY1 expression through miR-7 elevation, while miR-7 modulation in miR-7 SW620-CRHR2+ and miR-7 HCT116 cells, had opposite effects on YY1 and Fas expressions and cell sensitivity to CH11-killing. CRHR2/Ucn2 signaling is a negative regulator of CRC cell resistance to Fas/FasL-apoptosis via targeting the miR-7/YY1/Fas circuitry. CRHR2 restoration might prove effective in managing CRC response to immune-mediated apoptotic stimuli.
[Mh] Termos MeSH primário: Apoptose
Neoplasias Colorretais/patologia
Hormônio Liberador da Corticotropina/metabolismo
MicroRNAs/genética
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Urocortinas/metabolismo
Fator de Transcrição YY1/metabolismo
Receptor fas/metabolismo
[Mh] Termos MeSH secundário: Proliferação Celular
Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Hormônio Liberador da Corticotropina/genética
Transição Epitelial-Mesenquimal
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Receptores de Hormônio Liberador da Corticotropina/genética
Transdução de Sinais
Células Tumorais Cultivadas
Urocortinas/genética
Fator de Transcrição YY1/genética
Receptor fas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CRF receptor type 2); 0 (FAS protein, human); 0 (MIRN7 microRNA, human); 0 (MicroRNAs); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (UCN2 protein, human); 0 (Urocortins); 0 (YY1 Transcription Factor); 0 (YY1 protein, human); 0 (fas Receptor); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171214
[Lr] Data última revisão:
171214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.31064


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[PMID]:28938481
[Au] Autor:Myers B; McKlveen JM; Morano R; Ulrich-Lai YM; Solomon MB; Wilson SP; Herman JP
[Ad] Endereço:Biomedical Sciences, Colorado State University, Fort Collins, Colorado 80523.
[Ti] Título:Vesicular Glutamate Transporter 1 Knockdown in Infralimbic Prefrontal Cortex Augments Neuroendocrine Responses to Chronic Stress in Male Rats.
[So] Source:Endocrinology;158(10):3579-3591, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic stress-associated pathologies frequently associate with alterations in the structure and activity of the medial prefrontal cortex (mPFC). However, the influence of infralimbic cortex (IL) projection neurons on hypothalamic-pituitary-adrenal (HPA) axis activity is unknown, as is the involvement of these cells in chronic stress-induced endocrine alterations. In the current study, a lentiviral-packaged vector coding for a small interfering RNA (siRNA) targeting vesicular glutamate transporter (vGluT) 1 messenger RNA (mRNA) was microinjected into the IL of male rats. vGluT1 is responsible for presynaptic vesicular glutamate packaging in cortical neurons, and knockdown reduces the amount of glutamate available for synaptic release. After injection, rats were either exposed to chronic variable stress (CVS) or remained in the home cage as unstressed controls. Fifteen days after the initiation of CVS, all animals were exposed to a novel acute stressor (30-minute restraint) with blood collection for the analysis of adrenocorticotropic hormone (ACTH) and corticosterone. Additionally, brains were collected for in situ hybridization of corticotrophin-releasing hormone mRNA. In previously unstressed rats, vGluT1 siRNA significantly enhanced ACTH and corticosterone secretion. Compared with CVS animals receiving the green fluorescent protein control vector, the vGluT1 siRNA further increased basal and stress-induced corticosterone release. Further analysis revealed enhanced adrenal responsiveness in CVS rats treated with vGluT1 siRNA. Collectively, our results suggest that IL glutamate output inhibits HPA responses to acute stress and restrains corticosterone secretion during chronic stress, possibly at the level of the adrenal. Together, these findings pinpoint a neurochemical mechanism linking mPFC dysfunction with aberrant neuroendocrine responses to chronic stress.
[Mh] Termos MeSH primário: Hormônio Adrenocorticotrópico/metabolismo
Corticosterona/metabolismo
Hormônio Liberador da Corticotropina/genética
Córtex Pré-Frontal/metabolismo
RNA Mensageiro/metabolismo
Estresse Psicológico/metabolismo
Proteína Vesicular 1 de Transporte de Glutamato/genética
[Mh] Termos MeSH secundário: Animais
Técnicas de Silenciamento de Genes
Sistema Hipotálamo-Hipofisário/metabolismo
Imuno-Histoquímica
Hibridização In Situ
Masculino
Sistema Hipófise-Suprarrenal/metabolismo
RNA Interferente Pequeno
Radioimunoensaio
Ratos
Ratos Sprague-Dawley
Restrição Física
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (Slc17a7 protein, rat); 0 (Vesicular Glutamate Transport Protein 1); 9002-60-2 (Adrenocorticotropic Hormone); 9015-71-8 (Corticotropin-Releasing Hormone); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00426


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[PMID]:28911133
[Au] Autor:Katugampola H; King PJ; Chatterjee S; Meso M; Duncan AJ; Achermann JC; Guasti L; Ghataore L; Taylor NF; Allen R; Marlene S; Aquilina J; Abbara A; Jaysena CN; Dhillo WS; Dunkel L; Sankilampi U; Storr HL
[Ad] Endereço:Centre for Endocrinology, William Harvey Research Institute, London, EC1M 6BQ, United Kingdom.
[Ti] Título:Kisspeptin Is a Novel Regulator of Human Fetal Adrenocortical Development and Function: A Finding With Important Implications for the Human Fetoplacental Unit.
[So] Source:J Clin Endocrinol Metab;102(9):3349-3359, 2017 Sep 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: The human fetal adrenal (HFA) is an integral component of the fetoplacental unit and important for the maintenance of pregnancy. Low kisspeptin levels during pregnancy are associated with miscarriage, and kisspeptin and its receptor are expressed in the HFA. However, the role of kisspeptin in fetal adrenal function remains unknown. Objective: To determine the role of kisspeptin in the developing HFA. Design: Experiments using H295R and primary HFA cells as in vitro models of the fetal adrenal. Association of plasma kisspeptin levels with HFA size in a longitudinal clinical study. Setting: Academic research center and tertiary fetal medicine unit. Participants: Thirty-three healthy pregnant women were recruited at their 12-week routine antenatal ultrasound scan. Main Outcome Measures: The spatiotemporal expression of Kiss1R in the HFA. The production of dehydroepiandrosterone sulfate (DHEAS) from HFA cells after kisspeptin treatment, alone or in combination with adrenocorticotropic hormone or corticotropin-releasing hormone. Fetal adrenal volume (FAV) and kisspeptin levels at four antenatal visits (∼20, 28, 34, and 38 weeks' gestation). Results: Expression of Kiss1R was present in the HFA from 8 weeks after conception to term and was shown in the inner fetal zone. Kisspeptin significantly increased DHEAS production in H295R and second-trimester HFA cells. Serial measurements of kisspeptin confirmed a correlation with FAV growth in the second trimester, independent of sex or estimated fetal weight. Conclusions: Kisspeptin plays a key role in the regulation of the HFA and thus the fetoplacental unit, particularly in the second trimester of pregnancy.
[Mh] Termos MeSH primário: Córtex Suprarrenal/embriologia
Glândulas Suprarrenais/embriologia
Desenvolvimento Fetal/fisiologia
Kisspeptinas/sangue
[Mh] Termos MeSH secundário: Córtex Suprarrenal/crescimento & desenvolvimento
Glândulas Suprarrenais/crescimento & desenvolvimento
Hormônio Adrenocorticotrópico/metabolismo
Adulto
Análise de Variância
Biomarcadores/sangue
Hormônio Liberador da Corticotropina/metabolismo
Feminino
Seres Humanos
Gravidez
Resultado da Gravidez
Segundo Trimestre da Gravidez
Estudos Prospectivos
Ultrassonografia Pré-Natal
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (Kisspeptins); 9002-60-2 (Adrenocorticotropic Hormone); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171014
[Lr] Data última revisão:
171014
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00763


  9 / 11388 MEDLINE  
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[PMID]:28880949
[Au] Autor:Coplan JD; Gupta NK; Karim A; Rozenboym A; Smith ELP; Kral JG; Rosenblum LA
[Ad] Endereço:Department of Psychiatry and Behavioral Sciences, Biological Science Unit, State University of New York (SUNY) Downstate Medical Center, Brooklyn, New York, United States of America.
[Ti] Título:Maternal hypothalamic-pituitary-adrenal axis response to foraging uncertainty: A model of individual vs. social allostasis and the "Superorganism Hypothesis".
[So] Source:PLoS One;12(9):e0184340, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Food insecurity is a major global contributor to developmental origins of adult disease. The allostatic load of maternal food uncertainty from variable foraging demand (VFD) activates corticotropin-releasing factor (CRF) without eliciting hypothalamic-pituitary-adrenal (HPA) activation measured on a group level. Individual homeostatic adaptations of the HPA axis may subserve second-order homeostasis, a process we provisionally term "social allostasis." We postulate that maternal food insecurity induces a "superorganism" state through coordination of individual HPA axis response. METHODS: Twenty-four socially-housed bonnet macaque maternal-infant dyads were exposed to 16 weeks of alternating two-week epochs of low or high foraging demand shown to compromise normative maternal-infant rearing. Cerebrospinal fluid (CSF) CRF concentrations and plasma cortisol were measured pre- and post-VFD. Dyadic distance was measured, and blinded observers performed pre-VFD social ranking assessments. RESULTS: Despite marked individual cortisol responses (mean change = 20%) there was an absence of maternal HPA axis group mean response to VFD (0%). Whereas individual CSF CRF concentrations change = 56%, group mean did increase 25% (p = 0.002). Our "dyadic vulnerability" index (low infant weight, low maternal weight, subordinate maternal social status and reduced dyadic distance) predicted maternal cortisol decreases (p < 0.0001) whereas relatively "advantaged" dyads exhibited maternal cortisol increases in response to VFD exposure. COMMENT: In response to a chronic stressor, relative dyadic vulnerability plays a significant role in determining the directionality and magnitude of individual maternal HPA axis responses in the service of maintaining a "superorganism" version of HPA axis homeostasis, provisionally termed "social allostasis."
[Mh] Termos MeSH primário: Comportamento Alimentar/fisiologia
Macaca radiata/fisiologia
Comportamento Materno/fisiologia
[Mh] Termos MeSH secundário: Alostase
Animais
Hormônio Liberador da Corticotropina/sangue
Hormônio Liberador da Corticotropina/líquido cefalorraquidiano
Feminino
Hidrocortisona/sangue
Hidrocortisona/líquido cefalorraquidiano
Sistema Hipotálamo-Hipofisário/metabolismo
Sistema Hipotálamo-Hipofisário/fisiologia
Sistema Hipófise-Suprarrenal/metabolismo
Sistema Hipófise-Suprarrenal/fisiologia
Incerteza
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
9015-71-8 (Corticotropin-Releasing Hormone); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184340


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[PMID]:28871578
[Au] Autor:Seki T; Yasuda A; Oki M; Kitajima N; Takagi A; Nakajima N; Miyajima A; Fukagawa M
[Ad] Endereço:Division of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Tokai University School of Medicine, 143 Shimokasuya, Iseharashi, Kanagawa 259-1193, Japan. tsekimdpdd@tokai-u.jp.
[Ti] Título:Secondary Adrenal Insufficiency Following Nivolumab Therapy in a Patient with Metastatic Renal Cell Carcinoma.
[So] Source:Tokai J Exp Clin Med;42(3):115-120, 2017 Sep 20.
[Is] ISSN:2185-2243
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Currently, nivolumab (an anti-programmed cell death-1 receptor monoclonal antibody) is available for many types of advanced cancers in Japan. However, there have been few detailed case reports about endocrine-related adverse events of this therapy. Here, we report a patient with metastatic renal cell carcinoma who presented with secondary adrenal insufficiency following nivolumab therapy. Endocrinological assessment by rapid adrenocorticotropic hormone (ACTH) and corticotropin-releasing hormone (CRH) tests revealed that the patient's disorder was a secondary adrenal insufficiency due to pituitary dysfunction. Moreover, the results of the thyrotropin-releasing hormone (TRH), luteinizing hormone-releasing hormone (LH-RH) and growth hormone-releasing peptide-2 (GHRP-2) tests showed that only the ACTH function was destroyed (isolated ACTH deficiency). The magnetic resonance imaging (MRI) findings of hypophysitis, which is the major cause of isolated ACTH deficiency, usually demonstrate enlargement of the pituitary gland. However, the MRI findings of our case showed no abnormalities of the pituitary gland and stalk. Therefore, not only oncologists, but also other specialists, including doctors in emergency units, should have knowledge of this specific feature. Our clinical observation could be useful to avoid a delay in diagnosis and to treat life-threatening adverse effects of nivolumab therapy, such as secondary adrenal insufficiency.
[Mh] Termos MeSH primário: Insuficiência Adrenal/induzido quimicamente
Anticorpos Monoclonais/efeitos adversos
Antineoplásicos/efeitos adversos
Carcinoma de Células Renais/tratamento farmacológico
Neoplasias Renais/tratamento farmacológico
[Mh] Termos MeSH secundário: Insuficiência Adrenal/diagnóstico
Hormônio Adrenocorticotrópico/sangue
Idoso
Anticorpos Monoclonais/administração & dosagem
Antineoplásicos/administração & dosagem
Biomarcadores/sangue
Carcinoma de Células Renais/secundário
Hormônio Liberador da Corticotropina/sangue
Feminino
Seres Humanos
Hiponatremia/induzido quimicamente
Hipofisite/complicações
Hipofisite/diagnóstico por imagem
Infusões Intravenosas
Neoplasias Renais/secundário
Imagem por Ressonância Magnética
Doenças da Hipófise/complicações
Doenças da Hipófise/diagnóstico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antineoplastic Agents); 0 (Biomarkers); 31YO63LBSN (nivolumab); 9002-60-2 (Adrenocorticotropic Hormone); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE



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