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[PMID]:28456768
[Au] Autor:Skorzewska A; Wislowska-Stanek A; Lehner M; Turzynska D; Sobolewska A; Krzascik P; Plaznik A
[Ad] Endereço:Department of Neurochemistry, Institute of Psychiatry and Neurology, Warsaw, Poland. skorzews@ipin.edu.pl.
[Ti] Título:Corticotropin releasing factor receptor 1 antagonist differentially inhibits freezing behavior and changes gamma-aminobutyric acidergic activity in the amygdala in low- and high-anxiety rats.
[So] Source:J Physiol Pharmacol;68(1):35-46, 2017 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to examine the effects of non-peptide corticotropin-releasing factor receptor 1 (CRF ) antagonist (antalarmin) administration on rat conditioned fear responses and gamma-aminobutyric acid (GABA)-ergic brain activity (GAD67 expression and GABA concentration) in low-anxiety (LR) and high-anxiety (HR) rats. The animals were divided into the LR and HR groups based on the duration of their conditioned freezing response in the first contextual fear test. After 28 days, the animals were re-subjected to the contextual fear training and test. The rats received an antalarmin injection (10 mg/kg or 20 mg/kg) 80 min before the second exposure to the aversive context. Antalarmin significantly attenuated the conditioned fear response only in the HR rats. The behavioral effect of a lower dose (10 mg/kg) of antalarmin was accompanied by increased GAD67 expression in the prelimbic cortex (PL) and central nucleus of the amygdala (CeA) and an increased GABA concentration in the amygdala. These studies showed that HR rats were more susceptible to the anxiolytic effects of CRF antagonist administration, which were associated with increased GABAergic activity in the medial prefrontal cortex and amygdala. The current data may provide insights into the neurobiological mechanism operating within the mesolimbic CRF-GABA neurotransmitter systems, which may be responsible for individual differences in stress-related diseases. This knowledge can be applied to further elucidate the pathophysiology of anxiety and trauma/stress-related disorders.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/efeitos dos fármacos
Ansiedade/metabolismo
Reação de Congelamento Cataléptica/efeitos dos fármacos
Córtex Pré-Frontal/efeitos dos fármacos
Pirimidinas/farmacologia
Pirróis/farmacologia
Receptores de Hormônio Liberador da Corticotropina/antagonistas & inibidores
[Mh] Termos MeSH secundário: Tonsila do Cerebelo/metabolismo
Animais
Comportamento Animal/efeitos dos fármacos
Condicionamento Clássico
Medo
Glutamato Descarboxilase/metabolismo
Masculino
Córtex Pré-Frontal/metabolismo
Ratos Wistar
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CRF receptor type 1); 0 (Pyrimidines); 0 (Pyrroles); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (antalarmin); 56-12-2 (gamma-Aminobutyric Acid); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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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


  3 / 2697 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


  4 / 2697 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


  5 / 2697 MEDLINE  
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[PMID]:28750017
[Au] Autor:Zhang C; Rissman RA
[Ad] Endereço:Department of Neurosciences, University of California, San Diego School of Medicine, La Jolla, California, United States of America.
[Ti] Título:Corticotropin-releasing factor receptor-1 modulates biomarkers of DNA oxidation in Alzheimer's disease mice.
[So] Source:PLoS One;12(7):e0181367, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Increased production of hydroxyl radical is the main source of oxidative damage in mammalian DNA that accumulates in Alzheimer's disease (AD). Reactive oxygen species (ROS) react with both nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) to generate 8-hydroxy-2'-deoxyguanosine (8-OHdG), both of which can be measured in the urine. Knowledge of this pathway has positioned measurement of urine 8-OHdG as a reliable index of DNA oxidation and a potential biomarker target for tracking early cellular dysfunction in AD. Furthermore, epigenetic studies demonstrate decreased global DNA methylation levels (e.g. 5-methyl-2'-deoxycytidine, 5-mdC) in AD tissues. Moreover, stress hormones can activate neuronal oxidative stress which will stimulate the release of additional stress hormones and result in damages to hippocampal neurons in the AD brain. Our previous work suggests that treating AD transgenic mice the type-1 corticotropin-releasing factor receptor (CRFR1) antagonist, R121919, to reduce stress signaling, prevented onset of cognitive impairment, synaptic/dendritic loss and Aß plaque accumulation. Therefore, to investigate whether levels of DNA oxidation can be impacted by the same therapeutic approach, urine levels of hydrogen peroxide, 8-OHdG, 5-mdC and total antioxidant capacity (TAC) were analyzed using an AD Tg mouse model. We found that Tg animals had an 80% increase in hydrogen peroxide levels compared to wild type (Wt) counterparts, an effect that could be dramatically reversed by the chronic administration with R121919. A significant decrease of 8-OHdG levels was observed in Tg mice treated with CRFR1 antagonist. Collectively our data suggest that the beneficial effects of CRFR1 antagonism seen in Tg mice may be mechanistically linked to the modulation of oxidative stress pathways.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Biomarcadores/metabolismo
DNA/metabolismo
Receptores de Hormônio Liberador da Corticotropina/metabolismo
[Mh] Termos MeSH secundário: Doença de Alzheimer/sangue
Doença de Alzheimer/urina
Animais
Antioxidantes/metabolismo
Comportamento Animal/efeitos dos fármacos
Biomarcadores/sangue
Biomarcadores/urina
Desoxicitidina/análogos & derivados
Desoxicitidina/urina
Desoxiguanosina/análogos & derivados
Desoxiguanosina/metabolismo
Ensaio de Imunoadsorção Enzimática
Feminino
Peróxido de Hidrogênio/metabolismo
Peróxido de Hidrogênio/urina
Masculino
Camundongos Transgênicos
Oxirredução/efeitos dos fármacos
Pirimidinas/química
Pirimidinas/farmacologia
Receptores de Hormônio Liberador da Corticotropina/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Biomarkers); 0 (CRF receptor type 1); 0 (Pyrimidines); 0 (R 121919); 0 (Receptors, Corticotropin-Releasing Hormone); 0W860991D6 (Deoxycytidine); 88847-89-6 (8-oxo-7-hydrodeoxyguanosine); 9007-49-2 (DNA); B200GV71QM (5-methyldeoxycytidine); BBX060AN9V (Hydrogen Peroxide); G9481N71RO (Deoxyguanosine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181367


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[PMID]:28628658
[Au] Autor:Bethea CL; Mueller K; Reddy AP; Kohama SG; Urbanski HF
[Ad] Endereço:Division of Reproductive and Developmental Science, Oregon National Primate Research Center, Beaverton, OR, United States of America.
[Ti] Título:Effects of obesogenic diet and estradiol on dorsal raphe gene expression in old female macaques.
[So] Source:PLoS One;12(6):e0178788, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The beneficial effects of bioidentical ovarian steroid hormone therapy (HT) during the perimenopause are gaining recognition. However, the positive effects of estrogen (E) plus or minus progesterone (P) administration to ovariectomized (Ovx) lab animals were recognized in multiple systems for years before clinical trials could adequately duplicate the results. Moreover, very large numbers of women are often needed to find statistically significant results in clinical trials of HT; and there are still opposing results being published, especially in neural and cardiovascular systems. One of the obvious differences between human and animal studies is diet. Laboratory animals are fed a diet that is low in fat and refined sugar, but high in micronutrients. In the US, a large portion of the population eats what is known as a "western style diet" or WSD that provides calories from 36% fat, 44% carbohydrates (includes 18.5% sugars) and 18% protein. Unfortunately, obesity and diabetes have reached epidemic proportions and the percentage of obese women in clinical trials may be overlooked. We questioned whether WSD and obesity could decrease the positive neural effects of estradiol (E) in the serotonin system of old macaques that were surgically menopausal. Old ovo-hysterectomized female monkeys were fed WSD for 2.5 years, and treated with placebo, Immediate E (ImE) or Delayed E (DE). Compared to old Ovx macaques on primate chow and treated with placebo or E, the WSD-fed monkeys exhibited greater individual variance and blunted responses to E-treatment in the expression of genes related to serotonin neurotransmission, CRH components in the midbrain, synapse assembly, DNA repair, protein folding, ubiquitylation, transport and neurodegeneration. For many of the genes examined, transcript abundance was lower in WSD-fed than chow-fed monkeys. In summary, an obesogenic diet for 2.5 years in old surgically menopausal macaques blunted or increased variability in E-induced gene expression in the dorsal raphe. These results suggest that with regard to function and viability in the dorsal raphe, HT may not be as beneficial for obese women as normal weight women.
[Mh] Termos MeSH primário: Dieta Ocidental
Núcleo Dorsal da Rafe/efeitos dos fármacos
Estradiol/farmacologia
Macaca mulatta/metabolismo
[Mh] Termos MeSH secundário: Animais
Moléculas de Adesão Celular Neuronais/genética
Moléculas de Adesão Celular Neuronais/metabolismo
DNA Liase (Sítios Apurínicos ou Apirimidínicos)/genética
DNA Liase (Sítios Apurínicos ou Apirimidínicos)/metabolismo
Núcleo Dorsal da Rafe/metabolismo
Feminino
Histerectomia
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Mesencéfalo/metabolismo
Chaperonas Moleculares/genética
Chaperonas Moleculares/metabolismo
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Ovariectomia
Receptores de Hormônio Liberador da Corticotropina/genética
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Serotonina/genética
Serotonina/metabolismo
Sinapses/metabolismo
Ubiquitina/genética
Ubiquitina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules, Neuronal); 0 (Membrane Proteins); 0 (Molecular Chaperones); 0 (Nerve Tissue Proteins); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (Ubiquitin); 0 (neuroligin 3); 333DO1RDJY (Serotonin); 4TI98Z838E (Estradiol); EC 4.2.99.18 (DNA-(Apurinic or Apyrimidinic Site) Lyase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178788


  7 / 2697 MEDLINE  
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[PMID]:28618089
[Au] Autor:Fang X; Hong Y; Dai L; Qian Y; Zhu C; Wu B; Li S
[Ad] Endereço:Department of Pharmacology, Nanjing Medical University, Nanjing, China.
[Ti] Título:CRH promotes human colon cancer cell proliferation via IL-6/JAK2/STAT3 signaling pathway and VEGF-induced tumor angiogenesis.
[So] Source:Mol Carcinog;56(11):2434-2445, 2017 Nov.
[Is] ISSN:1098-2744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Corticotrophin-releasing hormone (CRH) has been demonstrated to participate in various diseases. Our previous study showed that its receptor CRHR1 mediated the development of colitis-associated cancer in mouse model. However, the detailed mechanisms remain unclear. In this study, we explored the oncogenetic role of CRH/CRHR1 signaling in colon cancer cells. Cell proliferation and colony formation assays revealed that CRH contributed to cell proliferation. Moreover, tube formation assay showed that CRH-treated colon cancer cell supernatant significantly promoted tube formation of human umbilical vein endothelial cells (HUVECs). And these effects could be reversed by the CRHR1 specific antagonist Antalarmin. Further investigation showed that CRH significantly upregulated the expressions of interlukin-6 (IL-6) and vascular endothelial growth factor (VEGF) through activating nuclear factor-kappa B (NF-κB). The CRH-induced IL-6 promoted phosphorylation of janus kinase 2 (JAK2) and signal transducers and activators of transcription 3 (STAT3). STAT3 inhibition by Stattic significantly inhibited the CRH-induced cell proliferation. In addition, silence of VEGF resulted in declined tube formation induced by CRH. Taken together, CRH/CRHR1 signaling promoted human colon cancer cell proliferation via NF-κB/IL-6/JAK2/STAT3 signaling pathway and tumor angiogenesis via NF-κB/VEGF signaling pathway. Our results provide evidence to support a critical role for the CRH/CRHR1 signaling in colon cancer progression and suggest its potential utility as a new therapeutic target for colon cancer.
[Mh] Termos MeSH primário: Neoplasias do Colo/metabolismo
Neoplasias do Colo/patologia
Hormônio Liberador da Corticotropina/metabolismo
Neovascularização Patológica/metabolismo
Transdução de Sinais
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proliferação Celular
Colo/irrigação sanguínea
Colo/metabolismo
Colo/patologia
Neoplasias do Colo/irrigação sanguínea
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Interleucina-6/metabolismo
Janus Quinase 2/metabolismo
Neovascularização Patológica/patologia
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Fator de Transcrição STAT3/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CRF receptor type 1); 0 (Interleukin-6); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (STAT3 Transcription Factor); 0 (Vascular Endothelial Growth Factor A); 9015-71-8 (Corticotropin-Releasing Hormone); EC 2.7.10.2 (JAK2 protein, human); EC 2.7.10.2 (Janus Kinase 2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1002/mc.22691


  8 / 2697 MEDLINE  
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[PMID]:28562585
[Au] Autor:Jazayeri A; Rappas M; Brown AJH; Kean J; Errey JC; Robertson NJ; Fiez-Vandal C; Andrews SP; Congreve M; Bortolato A; Mason JS; Baig AH; Teobald I; Doré AS; Weir M; Cooke RM; Marshall FH
[Ad] Endereço:Heptares Therapeutics Ltd, BioPark, Broadwater Road, Welwyn Garden City, Hertfordshire AL7 3AX, UK.
[Ti] Título:Crystal structure of the GLP-1 receptor bound to a peptide agonist.
[So] Source:Nature;546(7657):254-258, 2017 06 08.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glucagon-like peptide 1 (GLP-1) regulates glucose homeostasis through the control of insulin release from the pancreas. GLP-1 peptide agonists are efficacious drugs for the treatment of diabetes. To gain insight into the molecular mechanism of action of GLP-1 peptides, here we report the crystal structure of the full-length GLP-1 receptor bound to a truncated peptide agonist. The peptide agonist retains an α-helical conformation as it sits deep within the receptor-binding pocket. The arrangement of the transmembrane helices reveals hallmarks of an active conformation similar to that observed in class A receptors. Guided by this structural information, we design peptide agonists with potent in vivo activity in a mouse model of diabetes.
[Mh] Termos MeSH primário: Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas
Receptor do Peptídeo Semelhante ao Glucagon 1/química
Peptídeos/química
Peptídeos/farmacologia
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Cristalografia por Raios X
Relação Dose-Resposta a Droga
Receptor do Peptídeo Semelhante ao Glucagon 1/metabolismo
Seres Humanos
Masculino
Camundongos
Modelos Moleculares
Peptídeos/metabolismo
Conformação Proteica
Ratos
Receptores de Hormônio Liberador da Corticotropina/química
Receptores de Glucagon/química
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CRF receptor type 1); 0 (Glucagon-Like Peptide-1 Receptor); 0 (Peptides); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (Receptors, Glucagon)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170601
[St] Status:MEDLINE
[do] DOI:10.1038/nature22800


  9 / 2697 MEDLINE  
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[PMID]:28550160
[Au] Autor:Tsuda T; Takefuji M; Wettschureck N; Kotani K; Morimoto R; Okumura T; Kaur H; Eguchi S; Sakaguchi T; Ishihama S; Kikuchi R; Unno K; Matsushita K; Ishikawa S; Offermanns S; Murohara T
[Ad] Endereço:Department of Cardiology, Nagoya University School of Medicine, Nagoya, Japan.
[Ti] Título:Corticotropin releasing hormone receptor 2 exacerbates chronic cardiac dysfunction.
[So] Source:J Exp Med;214(7):1877-1888, 2017 Jul 03.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heart failure occurs when the heart is unable to effectively pump blood and maintain tissue perfusion. Despite numerous therapeutic advancements over previous decades, the prognosis of patients with chronic heart failure remains poor, emphasizing the need to identify additional pathophysiological factors. Here, we show that corticotropin releasing hormone receptor 2 (Crhr2) is a G protein-coupled receptor highly expressed in cardiomyocytes and continuous infusion of the Crhr2 agonist, urocortin 2 (Ucn2), reduced left ventricular ejection fraction in mice. Moreover, plasma Ucn2 levels were 7.5-fold higher in patients with heart failure compared to those in healthy controls. Additionally, cardiomyocyte-specific deletion of Crhr2 protected mice from pressure overload-induced cardiac dysfunction. Mice treated with a Crhr2 antagonist lost maladaptive 3'-5'-cyclic adenosine monophosphate (cAMP)-dependent signaling and did not develop heart failure in response to overload. Collectively, our results indicate that constitutive Crhr2 activation causes cardiac dysfunction and suggests that Crhr2 blockade is a promising therapeutic strategy for patients with chronic heart failure.
[Mh] Termos MeSH primário: Insuficiência Cardíaca/metabolismo
Miócitos Cardíacos/metabolismo
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Idoso
Animais
Western Blotting
Células Cultivadas
AMP Cíclico/metabolismo
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Feminino
Expressão Gênica
Insuficiência Cardíaca/sangue
Insuficiência Cardíaca/fisiopatologia
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Meia-Idade
Miócitos Cardíacos/efeitos dos fármacos
Receptores de Hormônio Liberador da Corticotropina/agonistas
Receptores de Hormônio Liberador da Corticotropina/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Urocortinas/sangue
Urocortinas/farmacologia
Função Ventricular Esquerda/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CRF receptor type 2); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (Urocortins); E0399OZS9N (Cyclic AMP)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20161924


  10 / 2697 MEDLINE  
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[PMID]:28541004
[Au] Autor:Hussain Z; Kim HW; Huh CW; Lee YJ; Park H
[Ad] Endereço:Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
[Ti] Título:The Effect of Peripheral CRF Peptide and Water Avoidance Stress on Colonic and Gastric Transit in Guinea Pigs.
[So] Source:Yonsei Med J;58(4):872-877, 2017 Jul.
[Is] ISSN:1976-2437
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:Functional dyspepsia (FD) and irritable bowel syndrome (IBS) are common gastrointestinal (GI) diseases; however, there is frequent overlap between FD and IBS patients. Emerging evidence links the activation of corticotropin releasing factor (CRF) receptors with stress-related alterations of gastric and colonic motor function. Therefore, we investigated the effect of peripheral CRF peptide and water avoidance stress (WAS) on upper and lower GI transit in guinea pigs. Dosages 1, 3, and 10 µg/kg of CRF were injected intraperitoneally (IP) in fasted guinea pigs 30 minutes prior to the intragastric administration of charcoal mix to measure upper GI transit. Colonic transits in non-fasted guinea pigs were assessed by fecal pellet output assay after above IP CRF doses. Blockade of CRF receptors by Astressin, and its effect on GI transit was also analyzed. Guinea pigs were subjected to WAS to measure gastrocolonic transit in different sets of experiments. Dose 10 µg/kg of CRF significantly inhibited upper GI transit. In contrast, there was dose dependent acceleration of the colonic transit. Remarkably, pretreatment of astressin significantly reverses the effect of CRF peptide on GI transit. WAS significantly increase colonic transit, but failed to accelerate upper GI transit. Peripheral CRF peptide significantly suppressed upper GI transit and accelerated colon transit, while central CRF involved WAS stimulated only colonic transit. Therefore, peripheral CRF could be utilized to establish the animal model of overlap syndrome.
[Mh] Termos MeSH primário: Colo/fisiopatologia
Hormônio Liberador da Corticotropina/farmacologia
Desidratação/fisiopatologia
Trânsito Gastrointestinal/efeitos dos fármacos
Peptídeos/farmacologia
[Mh] Termos MeSH secundário: Animais
Colo/efeitos dos fármacos
Cobaias
Masculino
Fragmentos de Peptídeos/farmacologia
Receptores de Hormônio Liberador da Corticotropina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptide Fragments); 0 (Peptides); 0 (Receptors, Corticotropin-Releasing Hormone); 170809-51-5 (astressin); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.3349/ymj.2017.58.4.872



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