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[PMID]:28457941
[Au] Autor:Menazza S; Sun J; Appachi S; Chambliss KL; Kim SH; Aponte A; Khan S; Katzenellenbogen JA; Katzenellenbogen BS; Shaul PW; Murphy E
[Ad] Endereço:Systems Biology Center, National Heart Lung and Blood Institute, NIH, Bethesda, MD, United States.
[Ti] Título:Non-nuclear estrogen receptor alpha activation in endothelium reduces cardiac ischemia-reperfusion injury in mice.
[So] Source:J Mol Cell Cardiol;107:41-51, 2017 Jun.
[Is] ISSN:1095-8584
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Steroid hormone receptors including estrogen receptors (ER) classically function as ligand-regulated transcription factors. However, estrogens also elicit cellular effects through binding to extra-nuclear ER (ERα, ERß, and G protein-coupled ER or GPER) that are coupled to kinases. How extra-nuclear ER actions impact cardiac ischemia-reperfusion (I/R) injury is unknown. We treated ovariectomized wild-type female mice with estradiol or an estrogen-dendrimer conjugate (EDC), which selectively activates extra-nuclear ER, or vehicle interventions for two weeks. I/R injury was then evaluated in isolated Langendorff perfused hearts. Two weeks of treatment with estradiol significantly decreased infarct size and improved post-ischemic contractile function. Similarly, EDC treatment significantly decreased infarct size and increased post-ischemic functional recovery compared to vehicle-treated hearts. EDC also caused an increase in myocardial protein S-nitrosylation, consistent with previous studies showing a role for this post-translational modification in cardioprotection. In further support of a role for S-nitrosylation, inhibition of nitric oxide synthase, but not soluble guanylyl cyclase blocked the EDC mediated protection. The administration of ICI182,780, which is an agonist of G-protein coupled estrogen receptor (GPER) and an antagonist of ERα and ERß, did not result in protection; however, ICI182,780 significantly blocked EDC-mediated cardioprotection, indicating participation of ERα and/or ERß. In studies determining the specific ER subtype and cellular target involved, EDC decreased infarct size and improved functional recovery in mice lacking ERα in cardiomyocytes. In contrast, protection was lost in mice deficient in endothelial cell ERα. Thus, extra-nuclear ERα activation in endothelium reduces cardiac I/R injury in mice, and this likely entails increased protein S-nitrosylation. Since EDC does not stimulate uterine growth, in the clinical setting EDC-like compounds may provide myocardial protection without undesired uterotrophic and cancer-promoting effects.
[Mh] Termos MeSH primário: Receptor alfa de Estrogênio/genética
Receptor beta de Estrogênio/genética
Isquemia/genética
Traumatismo por Reperfusão/genética
[Mh] Termos MeSH secundário: Animais
Endotélio/metabolismo
Endotélio/patologia
Receptor alfa de Estrogênio/antagonistas & inibidores
Receptor beta de Estrogênio/antagonistas & inibidores
Estrogênios/genética
Estrogênios/metabolismo
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Isquemia/metabolismo
Isquemia/patologia
Camundongos
Ovariectomia
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Receptores Estrogênicos/antagonistas & inibidores
Receptores Acoplados a Proteínas-G/antagonistas & inibidores
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/patologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor alpha); 0 (Estrogen Receptor beta); 0 (Estrogens); 0 (GPR30 protein, mouse); 0 (Receptors, Estrogen); 0 (Receptors, G-Protein-Coupled)
[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:170502
[St] Status:MEDLINE


  2 / 20339 MEDLINE  
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[PMID]:28452704
[Au] Autor:Yan CH; Hahn S; McMahon D; Bonislawski D; Kennedy DW; Adappa ND; Palmer JN; Jiang P; Lee RJ; Cohen NA
[Ad] Endereço:Department of Otorhinolaryngology-Head and Neck Surgery, Division of Rhinology, University of Pennsylvania, Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
[Ti] Título:Nitric oxide production is stimulated by bitter taste receptors ubiquitously expressed in the sinonasal cavity.
[So] Source:Am J Rhinol Allergy;31(2):85-92, 2017 Mar 01.
[Is] ISSN:1945-8932
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Bitter taste receptors (T2R) have recently been demonstrated to contribute to sinonasal innate immunity. One T2R, T2R38, regulates mucosal defense against gram-negative organisms through nitric oxide (NO) production, which enhances mucociliary clearance and directly kills bacteria. To determine whether additional T2Rs contribute to this innate defense, we evaluated two other sinonasal T2Rs (T2R4 and T2R16) for regulation of NO production and expression within the human sinonasal cavity. METHODS: Primary human sinonasal cultures were stimulated with ligands specific to T2R4 and T2R16, colchicine and D-salicin, respectively. Cellular NO production was measured by intracellular 4-amino-5-methylamino-2',7'-difluorofluorescein diacetate fluorescence. For T2R expression mapping, sinonasal tissue was obtained from patients who underwent sinus surgery of the middle turbinate, maxillary sinus, ethmoid sinus, or sphenoid sinus. The expression of T2R4, T2R16, and T2R38 was evaluated by using immunofluorescence with validated antibodies. RESULTS: Similar to T2R38, T2R4 and T2R16 trigger NO production in a dose-dependent manner by using the canonical taste signaling pathway in response to stimulation with their respective ligands. All three receptors were expressed in the cilia of human epithelial cells of all regions in the sinonasal cavity. CONCLUSION: These three T2Rs signaled through the same NO-mediated antimicrobial pathway and were ubiquitously expressed in the sinonasal epithelium. Additional T2Rs besides T2R38 may play a role in sinonasal immune defense. Mapping of T2R expression demonstrated the potential widespread role of T2Rs in sinonasal defense, whereas the genetics of these T2Rs may contribute to our understanding of specific endotypes of chronic rhinosinusitis and develop into novel therapeutic targets.
[Mh] Termos MeSH primário: Infecções Bacterianas/imunologia
Mucosa Nasal/imunologia
Seios Paranasais/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
Rinite/imunologia
Sinusite/imunologia
Paladar
[Mh] Termos MeSH secundário: Bacteriólise
Células Cultivadas
Doença Crônica
Seres Humanos
Imunidade Inata
Depuração Mucociliar
Mucosa Nasal/microbiologia
Óxido Nítrico/metabolismo
Cultura Primária de Células
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, G-Protein-Coupled); 0 (taste receptors, type 2); 31C4KY9ESH (Nitric Oxide)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.2500/ajra.2017.31.4424


  3 / 20339 MEDLINE  
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[PMID]:29441914
[Au] Autor:Lei Z; Xudong W; Wei M
[Ti] Título:Effects of taurochenodeoxycholic acid on Ca /CaM signalling mediated by the TGR5 signalling pathway.
[So] Source:Pharmazie;71(7):390-393, 2016 Jul 07.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Taurochenodeoxycholic acid (TCDCA), a natural bioactive substance in animal bile, has anti-inflammatory and immunoregulatory effects. This study evaluates the effects of TCDCA on calcium/calmodulin (Ca2+/CaM) signalling mediated by G Protein Coupled Bile Acid Receptor 1 (TGR5) to provide preliminary information on the mechanism of TCDCA in immune regulation and also to benefit future research. After treatment of NR8383 and high TGR5 expression cell (TGR5-NR8383) with TCDCA (10-6 mol/L, 10-5 mol/L, and 10-4 mol/L) for 1 h, we measured TGR5 and CaM gene and protein levels by quantitative reverse transcription-polymerase chain reaction (qPCR) and western blotting, respectively. The inositol triphosphate (IP3) concentration was measured by Enzyme-linked Immunosorbent Assay (ELISA), and the Ca2+ concentration was measured by calcium fluorescent probe (Fluo-3 AM). The present study showed that the expression levels of IP3, Ca2+, and CaM in NR8383 cells were increased by TCDCA at concentrations ranging from 10-6 mol/L to 10-4 mol/L. TCDCA (10-4 mol/L) increased both the gene and protein expression of IP3and CaM through TGR5. TCDCA (10-4 mol/L or 10-5 mol/L) also increased the Ca2+ concentration via the TGR5 receptor. Our data suggest TCDCA activates Ca2+/CaM signalling via the TGR5 signalling pathway.
[Mh] Termos MeSH primário: Sinalização do Cálcio/efeitos dos fármacos
Calmodulina/efeitos dos fármacos
Receptores Acoplados a Proteínas-G/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Ácido Tauroquenodesoxicólico/farmacologia
[Mh] Termos MeSH secundário: Animais
Sinalização do Cálcio/genética
Calmodulina/biossíntese
Calmodulina/genética
Linhagem Celular
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Inositol 1,4,5-Trifosfato/metabolismo
RNA Mensageiro/biossíntese
RNA Mensageiro/genética
Ratos
Receptores Acoplados a Proteínas-G/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Calmodulin); 0 (GPBAR1 protein, human); 0 (RNA, Messenger); 0 (Receptors, G-Protein-Coupled); 516-35-8 (Taurochenodeoxycholic Acid); 85166-31-0 (Inositol 1,4,5-Trisphosphate)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6541


  4 / 20339 MEDLINE  
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[PMID]:28743231
[Au] Autor:Xu X; Li G; Li L; Su Z; Chen C
[Ad] Endereço:College of Life Sciences, Nanjing Agricultural University, Nanjing, 210095, China.
[Ti] Título:Genome-wide comparative analysis of putative Pth11-related G protein-coupled receptors in fungi belonging to Pezizomycotina.
[So] Source:BMC Microbiol;17(1):166, 2017 Jul 25.
[Is] ISSN:1471-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: G-protein coupled receptors (GPCRs) are the largest family of transmembrane receptors in fungi, where they play important roles in signal transduction. Among them, the Pth11-related GPCRs form a large and divergent protein family, and are only found in fungi in Pezizomycotina. However, the evolutionary process and potential functions of Pth11-related GPCRs remain largely unknown. RESULTS: Twenty genomes of fungi in Pezizomycotina covering different nutritional strategies were mined for putative Pth11-related GPCRs. Phytopathogens encode much more putative Pth11-related GPCRs than symbionts, saprophytes, or entomopathogens. Based on the phylogenetic tree, these GPCRs can be divided into nine clades, with each clade containing fungi in different taxonomic orders. Instead of fungi from the same order, those fungi with similar nutritional strategies were inclined to share orthologs of putative Pth11-related GPCRs. Most of the CFEM domain-containing Pth11-related GPCRs, which were only included in two clades, were detected in phytopathogens. Furthermore, many putative Pth11-related GPCR genes of phytopathogens were upregulated during invasive plant infection, but downregulated under biotic stress. The expressions of putative Pth11-related GPCR genes of saprophytes and entomopathogens could be affected by nutrient conditions, especially the carbon source. The gene expressions revealed that Pth11-related GPCRs could respond to biotic/abiotic stress and invasive plant infection with different expression patterns. CONCLUSION: Our results indicated that the Pth11-related GPCRs existed before the diversification of Pezizomycotina and have been gained and/or lost several times during the evolutionary process. Tandem duplications and trophic variations have been important factors in this evolution.
[Mh] Termos MeSH primário: Ascomicetos/genética
Proteínas Fúngicas/química
Genoma Fúngico
Receptores Acoplados a Proteínas-G/química
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Ascomicetos/química
Ascomicetos/classificação
Ascomicetos/metabolismo
Evolução Molecular
Proteínas Fúngicas/genética
Proteínas Fúngicas/metabolismo
Dados de Sequência Molecular
Filogenia
Receptores Acoplados a Proteínas-G/genética
Alinhamento de Sequência
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fungal Proteins); 0 (Receptors, G-Protein-Coupled)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1186/s12866-017-1076-5


  5 / 20339 MEDLINE  
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[PMID]:28453858
[Au] Autor:McCormack SE; Li D; Kim YJ; Lee JY; Kim SH; Rapaport R; Levine MA
[Ad] Endereço:Division of Endocrinology and Diabetes, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104.
[Ti] Título:Digenic Inheritance of PROKR2 and WDR11 Mutations in Pituitary Stalk Interruption Syndrome.
[So] Source:J Clin Endocrinol Metab;102(7):2501-2507, 2017 Jul 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Pituitary stalk interruption syndrome (PSIS, ORPHA95496) is a congenital defect of the pituitary gland characterized by the triad of a very thin/interrupted pituitary stalk, an ectopic (or absent) posterior pituitary gland, and hypoplasia or aplasia of the anterior pituitary gland. Complex genetic patterns of inheritance of this disorder are increasingly recognized. Objective: The objective of this study was to identify a genetic cause of PSIS in an affected child. Methods: Whole exome sequencing (WES) was performed by using standard techniques, with prioritized genetic variants confirmed via Sanger sequencing. To investigate the effects of one candidate variant on mutant WDR11 function, Western blotting and coimmunofluorescence were used to assess binding capacity, and leptomycin B exposure along with immunofluorescence was used to assess nuclear localization. Results: We describe a child who presented in infancy with combined pituitary hormone deficiencies and whose brain imaging demonstrated a small anterior pituitary, ectopic posterior pituitary, and a thin, interrupted stalk. WES demonstrated heterozygous missense mutations in two genes required for pituitary development, a known loss-of-function mutation in PROKR2 (c.253C>T;p.R85C) inherited from an unaffected mother, and a WDR11 (c.1306A>G;p.I436V) mutation inherited from an unaffected father. Mutant WDR11 loses its capacity to bind to its functional partner, EMX1, and to localize to the nucleus. Conclusions: WES in a child with PSIS and his unaffected family implicates a digenic mechanism of inheritance. In cases of hypopituitarism in which there is incomplete segregation of a monogenic genotype with the phenotype, the possibility that a second genetic locus is involved should be considered.
[Mh] Termos MeSH primário: Predisposição Genética para Doença
Hipopituitarismo/genética
Proteínas de Membrana/genética
Mutação
Hipófise/anormalidades
Proteínas Proto-Oncogênicas/genética
Receptores Acoplados a Proteínas-G/genética
Receptores de Peptídeos/genética
[Mh] Termos MeSH secundário: Exoma/genética
Genótipo
Heterozigoto
Seres Humanos
Hipopituitarismo/congênito
Hipopituitarismo/patologia
Recém-Nascido
Masculino
Linhagem
Síndrome
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (PROKR2 protein, human); 0 (Proto-Oncogene Proteins); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Peptide); 0 (WDR11 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00332


  6 / 20339 MEDLINE  
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[PMID]:28461104
[Au] Autor:Prokop S; Perry NA; Vishnivetskiy SA; Toth AD; Inoue A; Milligan G; Iverson TM; Hunyady L; Gurevich VV
[Ad] Endereço:Department of Physiology, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
[Ti] Título:Differential manipulation of arrestin-3 binding to basal and agonist-activated G protein-coupled receptors.
[So] Source:Cell Signal;36:98-107, 2017 Aug.
[Is] ISSN:1873-3913
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Non-visual arrestins interact with hundreds of different G protein-coupled receptors (GPCRs). Here we show that by introducing mutations into elements that directly bind receptors, the specificity of arrestin-3 can be altered. Several mutations in the two parts of the central "crest" of the arrestin molecule, middle-loop and C-loop, enhanced or reduced arrestin-3 interactions with several GPCRs in receptor subtype and functional state-specific manner. For example, the Lys139Ile substitution in the middle-loop dramatically enhanced the binding to inactive M muscarinic receptor, so that agonist activation of the M did not further increase arrestin-3 binding. Thus, the Lys139Ile mutation made arrestin-3 essentially an activation-independent binding partner of M , whereas its interactions with other receptors, including the ß -adrenergic receptor and the D and D dopamine receptors, retained normal activation dependence. In contrast, the Ala248Val mutation enhanced agonist-induced arrestin-3 binding to the ß -adrenergic and D dopamine receptors, while reducing its interaction with the D dopamine receptor. These mutations represent the first example of altering arrestin specificity via enhancement of the arrestin-receptor interactions rather than selective reduction of the binding to certain subtypes.
[Mh] Termos MeSH primário: Arrestinas/metabolismo
Receptores Acoplados a Proteínas-G/agonistas
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Arrestinas/química
Células COS
Bovinos
Cercopithecus aethiops
Sequência Conservada
Células HEK293
Seres Humanos
Lisina/metabolismo
Proteínas Mutantes/metabolismo
Mutação/genética
Ligação Proteica
Estrutura Secundária de Proteína
Rodopsina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arrestins); 0 (Mutant Proteins); 0 (Receptors, G-Protein-Coupled); 0 (arrestin3); 9009-81-8 (Rhodopsin); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  7 / 20339 MEDLINE  
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[PMID]:28449947
[Au] Autor:Bahouth SW; Nooh MM
[Ad] Endereço:Department of Pharmacology, The University of Tennessee Health Sciences Center, 71 S. Manassas, Memphis, TN 38103, USA. Electronic address: sbahouth@uthsc.edu.
[Ti] Título:Barcoding of GPCR trafficking and signaling through the various trafficking roadmaps by compartmentalized signaling networks.
[So] Source:Cell Signal;36:42-55, 2017 Aug.
[Is] ISSN:1873-3913
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Proper signaling by G protein coupled receptors (GPCR) is dependent on the specific repertoire of transducing, enzymatic and regulatory kinases and phosphatases that shape its signaling output. Activation and signaling of the GPCR through its cognate G protein is impacted by G protein-coupled receptor kinase (GRK)-imprinted "barcodes" that recruit ß-arrestins to regulate subsequent desensitization, biased signaling and endocytosis of the GPCR. The outcome of agonist-internalized GPCR in endosomes is also regulated by sequence motifs or "barcodes" within the GPCR that mediate its recycling to the plasma membrane or retention and eventual degradation as well as its subsequent signaling in endosomes. Given the vast number of diverse sequences in GPCR, several trafficking mechanisms for endosomal GPCR have been described. The majority of recycling GPCR, are sorted out of endosomes in a "sequence-dependent pathway" anchored around a type-1 PDZ-binding module found in their C-tails. For a subset of these GPCR, a second "barcode" imprinted onto specific GPCR serine/threonine residues by compartmentalized kinase networks was required for their efficient recycling through the "sequence-dependent pathway". Mutating the serine/threonine residues involved, produced dramatic effects on GPCR trafficking, indicating that they played a major role in setting the trafficking itinerary of these GPCR. While endosomal SNX27, retromer/WASH complexes and actin were required for efficient sorting and budding of all these GPCR, additional proteins were required for GPCR sorting via the second "barcode". Here we will review recent developments in GPCR trafficking in general and the human ß -adrenergic receptor in particular across the various trafficking roadmaps. In addition, we will discuss the role of GPCR trafficking in regulating endosomal GPCR signaling, which promote biochemical and physiological effects that are distinct from those generated by the GPCR signal transduction pathway in membranes.
[Mh] Termos MeSH primário: Transporte Proteico
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Animais
Endossomos/metabolismo
Retroalimentação Fisiológica
Seres Humanos
Processamento de Proteína Pós-Traducional
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, G-Protein-Coupled)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


  8 / 20339 MEDLINE  
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[PMID]:28455260
[Au] Autor:Mikolajczyk-Stecyna J; Malinowska AM; Chmurzynska A
[Ad] Endereço:Molecular Metabolism Laboratory, Department of Human Nutrition and Hygiene, Faculty of Food Sciences, Poznan University of Life Sciences, Wojska Polskiego 31, 60-624 Poznan, Poland. Electronic address: joanstec@up.poznan.pl.
[Ti] Título:TAS2R38 and CA6 genetic polymorphisms, frequency of bitter food intake, and blood biomarkers among elderly woman.
[So] Source:Appetite;116:57-64, 2017 09 01.
[Is] ISSN:1095-8304
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Taste sensitivity is one of the most important biological determinants of food choice. Three SNPs of the TAS2R38 gene (rs713598, rs1726866, and rs10246939) give rise to two common haplotypes: PAV and AVI. These haplotypes, as well as an SNP within the CA6 gene (rs2274333) that encodes carbonic anhydrase VI (CA6), correlate with bitterness perception. The extent of consumption of bitter food may influence some health outcomes. The aim of this study is thus to investigate the impact of the TAS2R38 and CA6 genetic polymorphisms on the choice of bitter food, BMI, blood lipoprotein, and glucose concentrations as well as systemic inflammation in elderly women. METHODS: The associations between the TAS2R38 diplotype, CA6 genotype, and the intake of bitter-tasting foods were studied in a group of 118 Polish women over 60 years of age. The intake of Brassica vegetables, grapefruit, and coffee was assessed using a food frequency questionnaire. Biochemical parameters were measured using the spectrophotometric method. Genotyping was performed using the high resolution melting method. RESULTS: We found a correlation between lipid profile, glucose and CRP levels, and frequency of bitter food intake. The AVI/AVI subjects drank coffee more frequently than did the PAV/PAV homozygotes, as did the A carriers of CA6 in comparison with the GG homozygotes. We also observed that simultaneous carriers of the PAV haplotype and A allele of TAS2R38 and CA6, respectively, choose white cabbage more frequent and had lower plasma levels of CRP and glucose than did AVI/AVI and GG homozygotes. CONCLUSIONS: In elderly women, the TAS2R38 and CA6 polymorphisms may affect the frequency of consumption of coffee and white cabbage, but not of other bitter-tasting foods.
[Mh] Termos MeSH primário: Anidrases Carbônicas/genética
Fenômenos Fisiológicos da Nutrição do Idoso
Preferências Alimentares
Polimorfismo de Nucleotídeo Único
Receptores Acoplados a Proteínas-G/genética
Percepção Gustatória/genética
[Mh] Termos MeSH secundário: Idoso
Alelos
Biomarcadores/sangue
Brassica
Anidrases Carbônicas/metabolismo
Citrus paradisi
Café
Feminino
Frutas
Frequência do Gene
Estudos de Associação Genética
Seres Humanos
Meia-Idade
Polônia
Receptores Acoplados a Proteínas-G/metabolismo
Autorrelato
Paladar
Verduras
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Coffee); 0 (Receptors, G-Protein-Coupled); 0 (taste receptors, type 2); EC 4.2.1.1 (Carbonic Anhydrases); EC 4.2.1.1 (carbonic anhydrase VI)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


  9 / 20339 MEDLINE  
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[PMID]:29360846
[Au] Autor:Yu X; Stallone JN; Heaps CL; Han G
[Ad] Endereço:Veterinary Physiology & Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, United States of America.
[Ti] Título:The activation of G protein-coupled estrogen receptor induces relaxation via cAMP as well as potentiates contraction via EGFR transactivation in porcine coronary arteries.
[So] Source:PLoS One;13(1):e0191418, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Estrogen exerts protective effects against cardiovascular diseases in premenopausal women, but is associated with an increased risk of both coronary heart disease and stroke in older postmenopausal women. Studies have shown that activation of the G-protein-coupled estrogen receptor 1 (GPER) can cause either relaxation or contraction of arteries. It is highly likely that these dual actions of GPER may contribute to the seemingly paradoxical effects of estrogen in regulating coronary artery function. The objective of this study was to test the hypothesis that activation of GPER enhances agonist-stimulated porcine coronary artery contraction via epidermal growth factor receptor (EGFR) transactivation and its downstream extracellular signal-regulated kinases (ERK1/2) pathway. Isometric tension studies and western blot were performed to determine the effect of GPER activation on coronary artery contraction. Our findings demonstrated that G-1 caused concentration-dependent relaxation of ET-1-induced contraction, while pretreatment of arterial rings with G-1 significantly enhanced ET-1-induced contraction. GPER antagonist, G-36, significantly inhibited both the G-1-induced relaxation effect and G-1-enhanced ET-1 contraction. Gallein, a Gßγ inhibitor, significantly increased G-1-induced relaxation, yet inhibited G-1-enhanced ET-1-mediated contraction. Similarly, inhibition of EGFR with AG1478 or inhibition of Src with phosphatase 2 further increased G-1-induced relaxation responses in coronary arteries, but decreased G-1-enhanced ET-1-induced contraction. Western blot experiments in porcine coronary artery smooth muscle cells (PCASMC) showed that G-1 increased tyrosine phosphorylation of EGFR, which was inhibited by AG-1478. Furthermore, enzyme-linked immunosorbent assays showed that the level of heparin-binding EGF (HB-EGF) released by ET-1 treatment increased two-fold; whereas pre-incubation with G-1 further increased ET-1-induced HB-EGF release to four-fold over control conditions. Lastly, the role of ERK1/2 was determined by applying the MEK inhibitor, PD98059, in isometric tension studies and detecting phospho-ERK1/2 in immunoblotting. PD98059 potentiated G-1-induced relaxation response, but blocked G-1-enhanced ET-1-induced contraction. By western blot, G-1 treatment decreased phospho-ERK1/2, however, in the presence of the adenylyl cyclase inhibitor, SQ22536, G-1 significantly increased ERK1/2 phosphorylation in PCASMC. These data demonstrate that activation of GPER induces relaxation via cAMP as well as contraction via a mechanism involving transactivation of EGFR and the phosphorylation of ERK1/2 in porcine coronary arteries.
[Mh] Termos MeSH primário: Vasos Coronários/fisiologia
Receptor do Fator de Crescimento Epidérmico/genética
Receptores Estrogênicos/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Vasos Coronários/efeitos dos fármacos
Ciclopentanos/farmacologia
Flavonoides/farmacologia
Seres Humanos
Técnicas In Vitro
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Modelos Cardiovasculares
Miócitos de Músculo Liso/metabolismo
Quinazolinas/farmacologia
Quinolinas/farmacologia
Receptores Acoplados a Proteínas-G/agonistas
Suínos
Ativação Transcricional
Tirfostinas/farmacologia
Vasodilatação/efeitos dos fármacos
Vasodilatação/genética
Vasodilatação/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanone); 0 (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one); 0 (Cyclopentanes); 0 (Flavonoids); 0 (Quinazolines); 0 (Quinolines); 0 (Receptors, Estrogen); 0 (Receptors, G-Protein-Coupled); 0 (Tyrphostins); 170449-18-0 (tyrphostin AG 1478); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191418


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[PMID]:29364921
[Au] Autor:Nowak M; Boos A; Kowalewski MP
[Ad] Endereço:Institute of Veterinary Anatomy, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland.
[Ti] Título:Luteal and hypophyseal expression of the canine relaxin (RLN) system during pregnancy: Implications for luteotropic function.
[So] Source:PLoS One;13(1):e0191374, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:By acting through its receptors (RXFP1, RXFP2), relaxin (RLN) exerts species-specific effects during pregnancy; possible luteotropic effects through stimulation of prolactin (PRL) release have been suggested. In the domestic dog (Canis lupus familiaris) serum PRL increases in pregnant bitches shortly after RLN appears in the circulation, and a possible functional relationship between the RLN and the PRL systems in regulating progesterone secretion has been implied. Therefore, here (Study 1) the luteal expression and localization of the RLN system was investigated by immunohistochemistry using custom-made antibodies and semi-quantitative PCR, at selected time points during gestation: pre-implantation (d. 8-12), post-implantation (d. 18-25), mid-gestation (d. 35-40) and at normal and antigestagen-induced luteolysis. Further, (Study 2) hypophyseal expression of the RLN system and its spatial association with PRL was assessed. Luteal expression of RLN, but not of its receptors, was time-dependent: it increased significantly following implantation towards mid-gestation and decreased at prepartum. Antigestagen treatment resulted in downregulation of RLN and RXFP2. Whereas RLN was localized in steroidogenic cells, RXFP1 and RXFP2 also stained strongly in macrophages and vascular endothelial cells. The RLN system was detected in the canine adenohypophysis and was co-localized with PRL in hypophyseal lactotrophs. The intraluteal RLN seems to be involved in regulating the canine corpus luteum (CL) in a time-dependent manner. The presence of RLN family members in the adenohypophysis implies their possible involvement in regulating the availability of PRL and other pituitary hormones.
[Mh] Termos MeSH primário: Corpo Lúteo/fisiologia
Hipófise/fisiologia
Relaxina/fisiologia
[Mh] Termos MeSH secundário: Animais
Manutenção do Corpo Lúteo/genética
Manutenção do Corpo Lúteo/fisiologia
Cães
Estrenos/farmacologia
Feminino
Expressão Gênica/efeitos dos fármacos
Imuno-Histoquímica
Modelos Biológicos
Gravidez
Prolactina/sangue
Prolactina/fisiologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Receptores Acoplados a Proteínas-G/genética
Receptores Acoplados a Proteínas-G/fisiologia
Receptores de Peptídeos/genética
Receptores de Peptídeos/fisiologia
Relaxina/sangue
Relaxina/genética
Especificidade da Espécie
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Estrenes); 0 (RNA, Messenger); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Peptide); 0 (relaxin receptors); 0UT4JLE1CM (aglepristone); 9002-62-4 (Prolactin); 9002-69-1 (Relaxin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191374



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