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Pesquisa : D12.644.276.860.887 [Categoria DeCS]
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  1 / 2801 MEDLINE  
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[PMID]:28974369
[Au] Autor:Ávila-Mendoza J; Pérez-Rueda E; Urban-Sosa V; Carranza M; Martínez-Moreno CG; Luna M; Arámburo C
[Ad] Endereço:Departamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, Campus Juriquilla, Universidad Nacional Autónoma de México, Querétaro, Qro. 76230, Mexico.
[Ti] Título:Characterization and distribution of GHRH, PACAP, TRH, SST and IGF1 mRNAs in the green iguana.
[So] Source:Gen Comp Endocrinol;255:90-101, 2018 Jan 01.
[Is] ISSN:1095-6840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The somatotropic axis (SA) regulates numerous aspects of vertebrate physiology such as development, growth, and metabolism and has influence on several tissues including neural, immune, reproductive and gastric tract. Growth hormone (GH) is a key component of SA, it is synthesized and released mainly by pituitary somatotrophs, although now it is known that virtually all tissues can express GH, which, in addition to its well-described endocrine roles, also has autocrine/paracrine/intracrine actions. In the pituitary, GH expression is regulated by several hypothalamic neuropeptides including GHRH, PACAP, TRH and SST. GH, in turn, regulates IGF1 synthesis in several target tissues, adding complexity to the system since GH effects can be exerted either directly or mediated by IGF1. In reptiles, little is known about the SA components and their functional interactions. The aim of this work was to characterize the mRNAs of the principal SA components in the green iguana and to develop the tools that allow the study of the structural and functional evolution of this system in reptiles. By employing RT-PCR and RACE, the cDNAs encoding for GHRH, PACAP, TRH, SST and IGF1 were amplified and sequenced. Results showed that these cDNAs coded for the corresponding protein precursors of 154, 170, 243, 113, and 131 amino acids, respectively. Of these, GHRH, PACAP, SST and IGF1 precursors exhibited a high structural conservation with respect to its counterparts in other vertebrates. On the other hand, iguana's TRH precursor showed 7 functional copies of mature TRH (pyr-QHP-NH ), as compared to 4 and 6 copies of TRH in avian and mammalian proTRH sequences, respectively. It was found that in addition to its primary production site (brain for GHRH, PACAP, TRH and SST, and liver for IGF1), they were also expressed in other peripheral tissues, i.e. testes and ovaries expressed all the studied mRNAs, whereas TRH and IGF1 mRNAs were observed ubiquitously in all tissues considered. These results show that the main SA components in reptiles of the Squamata Order maintain a good structural conservation among vertebrate phylogeny, and suggest important physiological interactions (endocrine, autocrine and/or paracrine) between them due to their wide peripheral tissue expression.
[Mh] Termos MeSH primário: Hormônio Liberador de Hormônio do Crescimento/genética
Iguanas/genética
Fator de Crescimento Insulin-Like I/genética
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/genética
Somatostatina/genética
Hormônio Liberador de Tireotropina/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Hormônio Liberador de Hormônio do Crescimento/química
Hormônio Liberador de Hormônio do Crescimento/metabolismo
Fator de Crescimento Insulin-Like I/química
Fator de Crescimento Insulin-Like I/metabolismo
Filogenia
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/química
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Somatostatina/química
Somatostatina/metabolismo
Hormônio Liberador de Tireotropina/química
Hormônio Liberador de Tireotropina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (RNA, Messenger); 51110-01-1 (Somatostatin); 5Y5F15120W (Thyrotropin-Releasing Hormone); 67763-96-6 (Insulin-Like Growth Factor I); 9034-39-3 (Growth Hormone-Releasing Hormone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE


  2 / 2801 MEDLINE  
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[PMID]:29324772
[Au] Autor:Contina A; Bridge ES; Ross JD; Shipley JR; Kelly JF
[Ad] Endereço:Oklahoma Biological Survey, University of Oklahoma, Norman, OK, United States of America.
[Ti] Título:Examination of Clock and Adcyap1 gene variation in a neotropical migratory passerine.
[So] Source:PLoS One;13(1):e0190859, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Complex behavioral traits, such as those making up a migratory phenotype, are regulated by multiple environmental factors and multiple genes. We investigated possible relationships between microsatellite variation at two candidate genes implicated in the control of migratory behavior, Clock and Adcyap1, and several aspects of migratory life-history and evolutionary divergence in the Painted Bunting (Passerina ciris), a species that shows wide variation in migratory and molting strategies across a disjunct distribution. We focused on Clock and Adcyap1 microsatellite variation across three Painted Bunting populations in Oklahoma, Louisiana, and North Carolina, and for the Oklahoma breeding population we used published migration tracking data on adult males to explore phenotypic variation in individual migratory behavior. We found no correlation between microsatellite allele size within either Clock and Adcyap1 relative to the initiation or duration of fall migration in adult males breeding in Oklahoma. We also show the lack of significant correlations with aspects of the migratory phenotype for the Louisiana population. Our research highlights the limitations of studying microsatellite allelic mutations that are of undetermined functional influence relative to complex behavioral phenotypes.
[Mh] Termos MeSH primário: Proteínas Aviárias/genética
Proteínas CLOCK/genética
Variação Genética
Repetições de Microssatélites
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/genética
Aves Canoras/genética
[Mh] Termos MeSH secundário: Alelos
Migração Animal
Animais
Evolução Biológica
Estudos de Associação Genética
Louisiana
Masculino
Muda/genética
Mutação
North Carolina
Oklahoma
Fenótipo
Aves Canoras/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Avian Proteins); 0 (Pituitary Adenylate Cyclase-Activating Polypeptide); EC 2.3.1.48 (CLOCK Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190859


  3 / 2801 MEDLINE  
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[PMID]:28759637
[Au] Autor:Eneman B; Elmonem MA; van den Heuvel LP; Khodaparast L; Khodaparast L; van Geet C; Freson K; Levtchenko E
[Ad] Endereço:Department of Pediatric Nephrology & Growth and Regeneration, University Hospitals Leuven, KU Leuven - University of Leuven, Leuven, Belgium.
[Ti] Título:Pituitary adenylate cyclase-activating polypeptide (PACAP) in zebrafish models of nephrotic syndrome.
[So] Source:PLoS One;12(7):e0182100, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pituitary adenylate cyclase-activating polypeptide (PACAP) is an inhibitor of megakaryopoiesis and platelet function. Recently, PACAP deficiency was observed in children with nephrotic syndrome (NS), associated with increased platelet count and aggregability and increased risk of thrombosis. To further study PACAP deficiency in NS, we used transgenic Tg(cd41:EGFP) zebrafish with GFP-labeled thrombocytes. We generated two models for congenital NS, a morpholino injected model targeting nphs1 (nephrin), which is mutated in the Finnish-type congenital NS. The second model was induced by exposure to the nephrotoxic compound adriamycin. Nephrin RNA expression was quantified and zebrafish embryos were live-screened for proteinuria and pericardial edema as evidence of renal impairment. Protein levels of PACAP and its binding-protein ceruloplasmin were measured and GFP-labeled thrombocytes were quantified. We also evaluated the effects of PACAP morpholino injection and the rescue effects of PACAP-38 peptide in both congenital NS models. Nephrin downregulation and pericardial edema were observed in both nephrin morpholino injected and adriamycin exposed congenital NS models. However, PACAP deficiency was demonstrated only in the adriamycin exposed condition. Ceruloplasmin levels and the number of GFP-labeled thrombocytes remained unchanged in both models. PACAP morpholino injections worsened survival rates and the edema phenotype in both congenital NS models while injection with human PACAP-38 could only rescue the adriamycin exposed model. We hereby report, for the first time, PACAP deficiency in a NS zebrafish model as a consequence of adriamycin exposure. However, distinct from the human congenital NS, both zebrafish models retained normal levels of ceruloplasmin and thrombocytes. We further extend the renoprotective effects of the PACAP-38 peptide against adriamycin toxicity in zebrafish.
[Mh] Termos MeSH primário: Proteínas de Membrana/metabolismo
Síndrome Nefrótica/metabolismo
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
Proteínas de Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Animais
Plaquetas/metabolismo
Ceruloplasmina/metabolismo
Doxorrubicina/toxicidade
Proteínas de Membrana/genética
Síndrome Nefrótica/etiologia
Síndrome Nefrótica/genética
Fragmentos de Peptídeos/farmacologia
Pericárdio/efeitos dos fármacos
Pericárdio/metabolismo
Pericárdio/patologia
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/química
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/genética
Peixe-Zebra
Proteínas de Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Peptide Fragments); 0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (Zebrafish Proteins); 0 (nephrin); 80168379AG (Doxorubicin); EC 1.16.3.1 (Ceruloplasmin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182100


  4 / 2801 MEDLINE  
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[PMID]:28701321
[Au] Autor:Barrett KT; Daubenspeck JA; Wilson RJA
[Ad] Endereço:Department of Physiology and Pharmacology, Hotchkiss Brain Institute and Alberta Children's Hospital Research Institute, University of Calgary, Calgary, Alberta, Canada; and.
[Ti] Título:Pituitary adenylate cyclase-activating polypeptide drives cardiorespiratory responses to heat stress in neonatal mice.
[So] Source:Am J Physiol Regul Integr Comp Physiol;313(4):R385-R394, 2017 Oct 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) has emerged as a principal and rate-limiting regulator of physiological stress responses in adult rodents and has been implicated in sudden infant death syndrome (SIDS). Recent studies show that PACAP plays a role in neonatal cardiorespiratory responses to hypoxia, hypercapnia, and hypothermia, but not hyperthermia, which is often associated with SIDS. Here we tested the hypothesis that, consistent with a role in SIDS, PACAP is involved in regulating the neonatal cardiorespiratory responses to severe heat. To address this, we used head-out plethysmography and surface ECG electrodes to study the cardiorespiratory physiology of conscious neonatal PACAP-null and wild-type mice at ambient temperatures of 32°C (baseline) and 40°C (heat stress). We also assessed body surface temperature as an indicator of cutaneous heat loss. Our results show that wild-type neonatal mice respond to heat stress by increasing ventilation ( = 0.007) and associated expired CO ( = 0.041), heart rate ( < 0.001), and cutaneous heat loss ( < 0.001). In PACAP-null neonates, this heat response is impaired, as indicated by a decrease in ventilation ( = 0.04) and associated expired CO ( = 0.006) and a blunted increase in heart rate ( = 0.001) and cutaneous heat loss ( = 0.0002). In addition, heart rate variability at baseline was lower in PACAP-null neonates than wild-type controls ( < 0.01). These results suggest that, during heat stress, PACAP is important for neonatal cardiorespiratory responses that help regulate body temperature. Abnormal PACAP regulation could, therefore, contribute to neonatal disorders in which the autonomic response to stress is impaired, such as SIDS.
[Mh] Termos MeSH primário: Regulação da Temperatura Corporal/fisiologia
Aptidão Cardiorrespiratória/fisiologia
Frequência Cardíaca/fisiologia
Resposta ao Choque Térmico/fisiologia
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Ativação Enzimática
Feminino
Masculino
Camundongos
Camundongos Knockout
Fatores Sexuais
Temperatura Cutânea/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pituitary Adenylate Cyclase-Activating Polypeptide)
[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:170714
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00118.2017


  5 / 2801 MEDLINE  
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[PMID]:28592413
[Au] Autor:Hardwick JC; Clason TA; Tompkins JD; Girard BM; Baran CN; Merriam LA; May V; Parsons RL
[Ad] Endereço:Department of Biology, Ithaca College, Ithaca, New York.
[Ti] Título:Recruitment of endosomal signaling mediates the forskolin modulation of guinea pig cardiac neuron excitability.
[So] Source:Am J Physiol Cell Physiol;313(2):C219-C227, 2017 Aug 01.
[Is] ISSN:1522-1563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Forskolin, a selective activator of adenylyl cyclase (AC), commonly is used to establish actions of G protein-coupled receptors (GPCRs) that are initiated primarily through activation of AC/cAMP signaling pathways. In the present study, forskolin was used to evaluate the potential role of AC/cAMP, which is a major signaling mechanism for the pituitary adenylate cyclase-activating polypeptide (PACAP)-selective PAC1 receptor, in the regulation of guinea pig cardiac neuronal excitability. Forskolin (5-10 µM) increases excitability in ~60% of the cardiac neurons. The forskolin-mediated increase in excitability was considered related to cAMP regulation of a cyclic nucleotide gated channel or via protein kinase A (PKA)/ERK signaling, mechanisms that have been linked to PAC1 receptor activation. However, unlike PACAP mechanisms, forskolin enhancement of excitability was not significantly reduced by treatment with cesium to block currents through hyperpolarization-activated nonselective cation channels ( ) or by treatment with PD98059 to block MEK/ERK signaling. In contrast, treatment with the clathrin inhibitor Pitstop2 or the dynamin inhibitor dynasore eliminated the forskolin-induced increase in excitability; treatments with the inactive Pitstop analog or PP2 treatment to inhibit Src-mediated endocytosis mechanisms were ineffective. The PKA inhibitor KT5702 significantly suppressed the forskolin-induced change in excitability; further, KT5702 and Pitstop2 reduced the forskolin-stimulated MEK/ERK activation in cardiac neurons. Collectively, the present results suggest that forskolin activation of AC/cAMP/PKA signaling leads to the recruitment of clathrin/dynamin-dependent endosomal transduction cascades, including MEK/ERK signaling, and that endosomal signaling is the critical mechanism underlying the forskolin-induced increase in cardiac neuron excitability.
[Mh] Termos MeSH primário: Adenilil Ciclases/metabolismo
Colforsina/administração & dosagem
Coração/efeitos dos fármacos
Miocárdio/metabolismo
Neurônios/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Carbazóis/administração & dosagem
Clatrina/efeitos dos fármacos
AMP Cíclico/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Endossomos/efeitos dos fármacos
Endossomos/metabolismo
Flavonoides/administração & dosagem
Cobaias
Seres Humanos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Miocárdio/patologia
Neurônios/metabolismo
Neurônios/patologia
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
Pirróis/administração & dosagem
Receptores Acoplados a Proteínas-G/metabolismo
Receptores de Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one); 0 (Carbazoles); 0 (Clathrin); 0 (Flavonoids); 0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (Pyrroles); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I); 1F7A44V6OU (Colforsin); 58HV29I28S (KT 5720); E0399OZS9N (Cyclic AMP); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 4.6.1.1 (Adenylyl Cyclases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1152/ajpcell.00094.2017


  6 / 2801 MEDLINE  
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[PMID]:28511915
[Au] Autor:Jiménez Garduño AM; Juárez-Hernández LJ; Polanco MJ; Tosatto L; Michelatti D; Arosio D; Basso M; Pennuto M; Musio C
[Ad] Endereço:Institute of Biophysics (IBF), Trento Unit, National Research Council (CNR), Via alla Cascata 56/C, 38123 Trento, Italy & Bruno Kessler Foundation (FBK), LabSSAH, Via alla Cascata 56/C, 38123 Trento, Italy.
[Ti] Título:Altered ionic currents and amelioration by IGF-1 and PACAP in motoneuron-derived cells modelling SBMA.
[So] Source:Biophys Chem;229:68-76, 2017 Oct.
[Is] ISSN:1873-4200
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy's disease, is a motor neuron disease caused by the expansion of a polymorphic CAG tandem repeat encoding a polyglutamine (polyQ) tract in the androgen receptor (AR) gene. SBMA is triggered by the binding of mutant AR to its natural ligands, testosterone and dihydrotestosterone (DHT). To investigate the neuronal alterations of motor neuron cell models of SBMA, we applied patch-clamp methods to verify how polyQ expansions in the AR alter cell ionic currents. We used mouse motoneuron-derived MN-1 cells expressing normal AR (MN24Q) and mutant AR (MN100Q treated cells with vehicle EtOH and DHT). We observed a reduction of the current flux mainly at depolarizing potentials in the DHT-treated cells, while the dissection of macroscopic currents showed single different cationic currents belonging to voltage-gated channels. Also, we treated the cells with IGF-1 and PACAP, which have previously been shown to protect MN-1 cells from the toxicity of mutant AR, and we found an amelioration of the altered currents. Our results suggest that the electrophysiological correlate of SBMA is a suitable reference point for the identification of disease symptoms and for future therapeutic targets.
[Mh] Termos MeSH primário: Potenciais de Ação/efeitos dos fármacos
Fator de Crescimento Insulin-Like I/farmacologia
Modelos Biológicos
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/farmacologia
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Linhagem Celular
Seres Humanos
Camundongos
Neurônios Motores/citologia
Neurônios Motores/efeitos dos fármacos
Neurônios Motores/metabolismo
Transtornos Musculares Atróficos/metabolismo
Transtornos Musculares Atróficos/patologia
Técnicas de Patch-Clamp
Peptídeos/metabolismo
Potássio/metabolismo
Receptores Androgênicos/genética
Receptores Androgênicos/metabolismo
Sequências de Repetição em Tandem/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptides); 0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (Receptors, Androgen); 26700-71-0 (polyglutamine); 67763-96-6 (Insulin-Like Growth Factor I); RWP5GA015D (Potassium); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170518
[St] Status:MEDLINE


  7 / 2801 MEDLINE  
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[PMID]:28490016
[Au] Autor:Ivic I; Fulop BD; Juhasz T; Reglodi D; Toth G; Hashimoto H; Tamas A; Koller A
[Ad] Endereço:Institute for Translational Medicine, University of Pecs, Pecs, Hungary.
[Ti] Título:Backup Mechanisms Maintain PACAP/VIP-Induced Arterial Relaxations in Pituitary Adenylate Cyclase-Activating Polypeptide-Deficient Mice.
[So] Source:J Vasc Res;54(3):180-192, 2017.
[Is] ISSN:1423-0135
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Pituitary adenylate cyclase-activating polypeptide (PACAP) is a multifunctional neuropeptide in the VIP/secretin/glucagon peptide superfamily. Two active forms, PACAP1-38 and PACAP1-27, act through G protein-coupled receptors, the PAC1 and VPAC1/2 receptors. Effects of PACAP include potent vasomotor activity. Vasomotor activity and organ-specific vasomotor effects of PACAP-deficient mice have not yet been investigated; thus, the assessment of its physiological importance in vasomotor functions is still missing. We hypothesized that backup mechanisms exist to maintain PACAP pathway activity in PACAP knockout (KO) mice. Thus, we investigated the vasomotor effects of exogenous vasoactive intestinal peptide (VIP) and PACAP polypeptides in PACAP wild-type (WT) and PACAP-deficient (KO) male mice. METHODS: Carotid and femoral arteries were isolated from 8- to 12-week-old male WT and PACAP-KO mice. Vasomotor responses were measured with isometric myography. RESULTS: In the arteries of WT mice the peptides induced relaxations, which were significantly greater to PACAP1-38 than to PACAP1-27 and VIP. In KO mice, PACAP1-38 did not elicit relaxation, whereas PACAP1-27 and VIP elicited significantly greater relaxation in KO mice than in WT mice. The specific PAC1R and VPAC1R antagonist completely blocked the PACAP-induced relaxations. CONCLUSION: Our data suggest that in PACAP deficiency, backup mechanisms maintain arterial relaxations to polypeptides, indicating an important physiological role for the PACAP pathway in the regulation of vascular tone.
[Mh] Termos MeSH primário: Artéria Carótida Primitiva/efeitos dos fármacos
Artéria Femoral/efeitos dos fármacos
Fragmentos de Peptídeos/farmacologia
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/deficiência
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/farmacologia
Peptídeo Intestinal Vasoativo/farmacologia
Vasodilatação/efeitos dos fármacos
Vasodilatadores/farmacologia
[Mh] Termos MeSH secundário: Animais
Artéria Carótida Primitiva/enzimologia
Relação Dose-Resposta a Droga
Artéria Femoral/enzimologia
Genótipo
Técnicas In Vitro
Masculino
Camundongos Knockout
Fenótipo
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/genética
Receptores de Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/agonistas
Receptores de Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/agonistas
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adcyap1 protein, mouse); 0 (Peptide Fragments); 0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I); 0 (Receptors, Vasoactive Intestinal Polypeptide, Type I); 0 (Vasodilator Agents); 37221-79-7 (Vasoactive Intestinal Peptide)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170511
[St] Status:MEDLINE
[do] DOI:10.1159/000457798


  8 / 2801 MEDLINE  
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[PMID]:28335564
[Au] Autor:Werling D; Banks WA; Salameh TS; Kvarik T; Kovacs LA; Vaczy A; Szabo E; Mayer F; Varga R; Tamas A; Toth G; Biro Z; Atlasz T; Reglodi D
[Ad] Endereço:Department of Anatomy, University of Pecs, Medical School, Pecs 7624, Hungary. doraw86@gmail.com.
[Ti] Título:Passage through the Ocular Barriers and Beneficial Effects in Retinal Ischemia of Topical Application of PACAP1-38 in Rodents.
[So] Source:Int J Mol Sci;18(3), 2017 Mar 21.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP) has two active forms, PACAP1-27 and PACAP1-38. Among the well-established actions are PACAP's neurotrophic and neuroprotective effects, which have also been proven in models of different retinopathies. The route of delivery is usually intravitreal in studies proving PACAP's retinoprotective effects. Recently, we have shown that PACAP1-27 delivered as eye drops in benzalkonium-chloride was able to cross the ocular barriers and exert retinoprotection in ischemia. Since PACAP1-38 is the dominant form of the naturally occurring PACAP, our aim was to investigate whether the longer form is also able to cross the barriers and exert protective effects in permanent bilateral common carotid artery occlusion (BCCAO), a model of retinal hypoperfusion. Our results show that radioactive PACAP1-38 eye drops could effectively pass through the ocular barriers to reach the retina. Routine histological analysis and immunohistochemical evaluation of the Müller glial cells revealed that PACAP1-38 exerted retinoprotective effects. PACAP1-38 attenuated the damage caused by hypoperfusion, apparent in almost all retinal layers, and it decreased the glial cell overactivation. Overall, our results confirm that PACAP1-38 given in the form of eye drops is a novel protective therapeutic approach to treat retinal diseases.
[Mh] Termos MeSH primário: Isquemia/tratamento farmacológico
Fármacos Neuroprotetores/farmacocinética
Fragmentos de Peptídeos/farmacocinética
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/farmacocinética
Doenças Retinianas/tratamento farmacológico
Vasos Retinianos/patologia
[Mh] Termos MeSH secundário: Animais
Camundongos
Fármacos Neuroprotetores/administração & dosagem
Fármacos Neuroprotetores/uso terapêutico
Soluções Oftálmicas
Fragmentos de Peptídeos/administração & dosagem
Fragmentos de Peptídeos/uso terapêutico
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/administração & dosagem
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/uso terapêutico
Ratos
Ratos Wistar
Retina/metabolismo
Vasos Retinianos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuroprotective Agents); 0 (Ophthalmic Solutions); 0 (Peptide Fragments); 0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (pituitary adenylate cyclase-activating-peptide (1-38), pig)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170425
[Lr] Data última revisão:
170425
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE


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[PMID]:28295336
[Au] Autor:Parker LM; Le S; Wearne TA; Hardwick K; Kumar NN; Robinson KJ; McMullan S; Goodchild AK
[Ad] Endereço:Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, NSW, 2109, Australia.
[Ti] Título:Neurochemistry of neurons in the ventrolateral medulla activated by hypotension: Are the same neurons activated by glucoprivation?
[So] Source:J Comp Neurol;525(9):2249-2264, 2017 Jun 15.
[Is] ISSN:1096-9861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous studies have demonstrated that a range of stimuli activate neurons, including catecholaminergic neurons, in the ventrolateral medulla. Not all catecholaminergic neurons are activated and other neurochemical content is largely unknown hence whether stimulus specific populations exist is unclear. Here we determine the neurochemistry (using in situ hybridization) of catecholaminergic and noncatecholaminergic neurons which express c-Fos immunoreactivity throughout the rostrocaudal extent of the ventrolateral medulla, in Sprague Dawley rats treated with hydralazine or saline. Distinct neuronal populations containing PPCART, PPPACAP, and PPNPY mRNAs, which were largely catecholaminergic, were activated by hydralazine but not saline. Both catecholaminergic and noncatecholaminergic neurons containing preprotachykinin and prepro-enkephalin (PPE) mRNAs were also activated, with the noncatecholaminergic population located in the rostral C1 region. Few GlyT2 neurons were activated. A subset of these data was then used to compare the neuronal populations activated by 2-deoxyglucose evoked glucoprivation (Brain Structure and Function (2015) 220:117). Hydralazine activated more neurons than 2-deoxyglucose but similar numbers of catecholaminergic neurons. Commonly activated populations expressing PPNPY and PPE mRNAs were defined. These likely include PPNPY expressing catecholaminergic neurons projecting to vasopressinergic and corticotrophin releasing factor neurons in the paraventricular nucleus, which when activated result in elevated plasma vasopressin and corticosterone. Stimulus specific neurons included noncatecholaminergic neurons and a few PPE positive catecholaminergic neuron but neurochemical codes were largely unidentified. Reasons for the lack of identification of stimulus specific neurons, readily detectable using electrophysiology in anaesthetized preparations and for which neural circuits can be defined, are discussed.
[Mh] Termos MeSH primário: Bulbo/citologia
Neuroquímica
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Hipertensivos/farmacologia
Catecolaminas/metabolismo
Desoxiglucose/farmacologia
Encefalinas/genética
Encefalinas/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Proteínas da Membrana Plasmática de Transporte de Glicina/genética
Proteínas da Membrana Plasmática de Transporte de Glicina/metabolismo
Hidralazina/farmacologia
Hipotensão/metabolismo
Hipotensão/patologia
Masculino
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Neuropeptídeo Y/genética
Neuropeptídeo Y/metabolismo
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/genética
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
Precursores de Proteínas/genética
Precursores de Proteínas/metabolismo
Proteínas Proto-Oncogênicas c-fos/genética
Proteínas Proto-Oncogênicas c-fos/metabolismo
Ratos
Ratos Sprague-Dawley
Taquicininas/genética
Taquicininas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adcyap1 protein, rat); 0 (Antihypertensive Agents); 0 (Catecholamines); 0 (Enkephalins); 0 (Glycine Plasma Membrane Transport Proteins); 0 (Nerve Tissue Proteins); 0 (Neuropeptide Y); 0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (Protein Precursors); 0 (Proto-Oncogene Proteins c-fos); 0 (Slc6a5 protein, rat); 0 (Tachykinins); 0 (cocaine- and amphetamine-regulated transcript protein); 0 (preprotachykinin); 26NAK24LS8 (Hydralazine); 93443-35-7 (preproenkephalin); 9G2MP84A8W (Deoxyglucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE
[do] DOI:10.1002/cne.24203


  10 / 2801 MEDLINE  
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[PMID]:28260603
[Au] Autor:Guo S
[Ad] Endereço:song.guo.01@regionh.dk.
[Ti] Título:The role of genetics on migraine induction triggered by CGRP and PACAP38.
[So] Source:Dan Med J;64(3), 2017 Mar.
[Is] ISSN:2245-1919
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Migraine has a strong genetic component and is characterized by multiphasic events including an initial premonitory phase with premonitory symptoms (PS). Calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating peptide-38 (PACAP38) are endogenous neuropeptides that can trigger migraine attacks and have in recent years gained considerable interest in the migraine field. Yet, the exact pathophysiological mechanisms underlying CGRP- and PACAP38-induced attacks are not fully clarified. Human provocation models have shown that these peptides induce attacks in only two- thirds of migraine patients. Whether this diverse migraine response after CGRP or PACAP38 may be explained by genetic factors is unknown. The present thesis includes four studies that explore different factors that may be associated with the CGRP- and PACAP38-induced migraine response. In study I and II we investigated the role of familial predisposition (family load) and number of risk conferring gene variants on migraine attacks induced by CGRP or PA-CAP38. In study III, we investigated biochemical changes of CGRP, vasoactive intestinal peptide (VIP), S100B and TNF-alpha in the blood after PACAP38. Finally in study IV, we studied whether CGRP or PACAP38 may induce PS. Study I and II demonstrated that PACAP38 and CGRP induce migraine attacks in 63% and 72% of the patients, respectively. Moreover, we showed that patients with high family load or a high number of migraine associated gene variants did not report more migraine attacks after CGRP or PACAP38 than those with no familial predisposition or few gene variants. Study III showed that PACAP38 infusion caused changes in plasma concentrations for VIP and S100B, but not CGRP and TNF-alpha, suggesting activation of parasympathetic nerve endings. Study IV showed absence of PS after CGRP and lack of statistical difference in PS between patients who reported and not reported attacks after PACAP38 suggesting peripheral mechanisms of induction. In conclusion, the present thesis suggests that genetics factors such as family load and genetic variants do not contribute to susceptibility of migraine attacks induced by CGRP or PACAP38. Additionally, our data indicate that CGRP and PACAP38 primarily have a peripheral site of action. We believe that the acquired knowledge from this thesis on how CGRP and PACAP38 might be involved in migraine pathophysiology would contribute to the development of novel and better migraine treatments in the future.
[Mh] Termos MeSH primário: Peptídeo Relacionado com Gene de Calcitonina/efeitos adversos
Transtornos de Enxaqueca/induzido quimicamente
Transtornos de Enxaqueca/genética
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Idoso
Peptídeo Relacionado com Gene de Calcitonina/administração & dosagem
Peptídeo Relacionado com Gene de Calcitonina/farmacologia
Feminino
Cefaleia/classificação
Cefaleia/fisiopatologia
Seres Humanos
Infusões Intravenosas
Masculino
Meia-Idade
Transtornos de Enxaqueca/sangue
Transtornos de Enxaqueca/fisiopatologia
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/administração & dosagem
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/farmacologia
Sintomas Prodrômicos
Ensaios Clínicos Controlados Aleatórios como Assunto
Fatores de Risco
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 83652-28-2 (Calcitonin Gene-Related Peptide)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170313
[Lr] Data última revisão:
170313
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170307
[St] Status:MEDLINE



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