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[PMID]:28465077
[Au] Autor:Malet M; Leiguarda C; Gastón G; McCarthy C; Brumovsky P
[Ad] Endereço:Instituto de Investigaciones en Medicina Traslacional (IIMT), Consejo Nacional de Investigaciones Cientiíficas y Técnicas (CONICET) - Austral University, Avenida Juan D. Perón 1500, B1629AHJ, Pilar, Buenos Aires, Argentina.
[Ti] Título:Spinal activation of the NPY Y1 receptor reduces mechanical and cold allodynia in rats with chronic constriction injury.
[So] Source:Peptides;92:38-45, 2017 Jun.
[Is] ISSN:1873-5169
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuropeptide tyrosine (NPY) and its associated receptors Y1R and Y2R have been previously implicated in the spinal modulation of neuropathic pain induced by total or partial sectioning of the sciatic nerve. However, their role in chronic constrictive injuries of the sciatic nerve has not yet been described. In the present study, we analyzed the consequences of pharmacological activation of spinal Y1R, by using the specific Y1R agonist Leu Pro -NPY, in rats with chronic constriction injury (CCI). CCI and sham-injury rats were implanted with a permanent intrathecal catheter (at day 7 after injury), and their response to the administration of different doses (2.5, 5, 7, 10 or 20µg) of Leu Pro -NPY (at a volume of 10µl) through the implanted catheter, recorded 14days after injury. Mechanical allodynia was tested by means of the up-and-down method, using von Frey filaments. Cold allodynia was tested by application of an acetone drop to the affected hindpaw. Intrathecal Leu Pro -NPY induced an increase of mechanical thresholds in rats with CCI, starting at doses of 5µg and becoming stronger with higher doses. Intrathecal Leu Pro also resulted in reductions in the frequency of withdrawal to cold stimuli, although the effect was somewhat more moderate and mostly observed for doses of 7µg and higher. We thus show that spinal activation of the Y1R is able to reduce neuropathic pain due to a chronic constrictive injury and, together with other studies, support the use of a spinal Y1R agonist as a therapeutic agent against chronic pain induced by peripheral neuropathy.
[Mh] Termos MeSH primário: Hiperalgesia/metabolismo
Neuropeptídeo Y/metabolismo
Receptores de Neuropeptídeo Y/metabolismo
Nervo Isquiático/lesões
Neuropatia Ciática/metabolismo
Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Dor Crônica/metabolismo
Temperatura Baixa
Constrição Patológica/complicações
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Hiperalgesia/etiologia
Injeções Espinhais
Masculino
Neuralgia/metabolismo
Medição da Dor
Limiar da Dor
Ratos
Ratos Sprague-Dawley
Receptores de Neuropeptídeo Y/agonistas
Neuropatia Ciática/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuropeptide Y); 0 (Receptors, Neuropeptide Y)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:28977590
[Au] Autor:Foradori CD; Whitlock BK; Daniel JA; Zimmerman AD; Jones MA; Read CC; Steele BP; Smith JT; Clarke IJ; Elsasser TH; Keisler DH; Sartin JL
[Ad] Endereço:Department of Anatomy, Physiology & Pharmacology, Auburn University, Auburn, Alabama 36849.
[Ti] Título:Kisspeptin Stimulates Growth Hormone Release by Utilizing Neuropeptide Y Pathways and Is Dependent on the Presence of Ghrelin in the Ewe.
[So] Source:Endocrinology;158(10):3526-3539, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although kisspeptin is the primary stimulator of gonadotropin-releasing hormone secretion and therefore the hypothalamic-pituitary-gonadal axis, recent findings suggest kisspeptin can also regulate additional neuroendocrine processes including release of growth hormone (GH). Here we show that central delivery of kisspeptin causes a robust rise in plasma GH in fasted but not fed sheep. Kisspeptin-induced GH secretion was similar in animals fasted for 24 hours and those fasted for 72 hours, suggesting that the factors involved in kisspeptin-induced GH secretion are responsive to loss of food availability and not the result of severe negative energy balance. Pretreatment with the neuropeptide Y (NPY) Y1 receptor antagonist, BIBO 3304, blocked the effects of kisspeptin-induced GH release, implicating NPY as an intermediary. Kisspeptin treatment induced c-Fos in NPY and GH-releasing hormone (GHRH) cells of the arcuate nucleus. The same kisspeptin treatment resulted in a reduction in c-Fos in somatostatin (SS) cells in the periventricular nucleus. Finally, blockade of systemic ghrelin release or antagonism of the ghrelin receptor eliminated or reduced the ability of kisspeptin to induce GH release, suggesting the presence of ghrelin is required for kisspeptin-induced GH release in fasted animals. Our findings support the hypothesis that during short-term fasting, systemic ghrelin concentrations and NPY expression in the arcuate nucleus rise. This permits kisspeptin activation of NPY cells. In turn, NPY stimulates GHRH cells and inhibits SS cells, resulting in GH release. We propose a mechanism by which kisspeptin conveys reproductive and hormone status onto the somatotropic axis, resulting in alterations in GH release.
[Mh] Termos MeSH primário: Grelina/metabolismo
Hormônio do Crescimento/efeitos dos fármacos
Kisspeptinas/farmacologia
Neuropeptídeo Y/metabolismo
Células Secretoras de Somatostatina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Núcleo Arqueado do Hipotálamo/efeitos dos fármacos
Núcleo Arqueado do Hipotálamo/metabolismo
Arginina/análogos & derivados
Arginina/farmacologia
Atropina/farmacologia
Jejum/metabolismo
Feminino
Imunofluorescência
Hormônio do Crescimento/secreção
Hormônio Liberador de Hormônio do Crescimento
Antagonistas Muscarínicos/farmacologia
Oligopeptídeos/farmacologia
Proteínas Proto-Oncogênicas c-fos/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-fos/metabolismo
Receptores de Grelina/antagonistas & inibidores
Receptores de Neuropeptídeo Y/antagonistas & inibidores
Ovinos
Carneiro Doméstico
Células Secretoras de Somatostatina/secreção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GHRP-6, Lys(3)-); 0 (Ghrelin); 0 (Kisspeptins); 0 (Muscarinic Antagonists); 0 (Neuropeptide Y); 0 (Oligopeptides); 0 (Proto-Oncogene Proteins c-fos); 0 (Receptors, Ghrelin); 0 (Receptors, Neuropeptide Y); 7C0697DR9I (Atropine); 9002-72-6 (Growth Hormone); 9034-39-3 (Growth Hormone-Releasing Hormone); 94ZLA3W45F (Arginine); O35HK034KO (BIBO 3304)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00303


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[PMID]:28864114
[Au] Autor:Ding X; Kou X; Zhang Y; Zhang X; Cheng G; Jia T
[Ad] Endereço:Department of internal neurology, Henan women and children health Hospital, Affiliated hospital of Zhengzhou University, Zhengzhou 450000, PR China.
[Ti] Título:Leptin siRNA promotes ovarian granulosa cell apoptosis and affects steroidogenesis by increasing NPY2 receptor expression.
[So] Source:Gene;633:28-34, 2017 Oct 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Leptin has been found to be involved in the ovarian granulosa cell apoptosis and steroidogenesis. Loss of neuropeptide Y (NPY) can correct the obesity syndrome of mutant mice lacking of leptin (ob/ob). However, the association of NPY and leptin in ovarian granulosa cells and ovarian steroidogenesis has not been investigated. Here, C57BL/6J ob/ob mice and C57BL/6J (control) mice were intraperitoneally injected with PBS, leptin (0.4µg/g bodyweight) or BIIE0246 (NPY2 receptor [NPY2R] antagonist, 30µg/kg bodyweight) every day for 15days. We found that NPY2R mRNA expression in mouse ovary was suppressed by leptin treatment, but increased by leptin deficiency. Leptin or BIIE0246 treatment significantly increased E2, but notably decreased progesterone in both mice. A lower level of E2 and a higher level of progesterone was observed in ob/ob mice than in control mice. Further, we then knocked down leptin expression in human ovarian granulosa cells by siRNA transfection and treated the cells with DMSO or BIIE0246. In vitro experiments confirmed the findings in mice. siLeptin treatment decreased the secretion of E2, anti-Mullerian hormone (AMH), insulin-like growth factor (IGF)-1 and transforming growth factor (TGF)-ß, and the cell proliferation, but increased the secretion of progesterone and cell apoptosis. Western blotting analysis of PCNA, Bcl-2 and Bax confirmed the results of cell proliferation and apoptosis. Activation of JAK2 and STAT3 was also suppressed by knocking down leptin. All the effects of siLeptin on ovarian granulosa cells were partially reversed by BIIE0246. In conclusion, knockdown of leptin significantly affected ovarian steroidogenesis and ovarian function through NPY. siLeptin transfection impaired the activation of JAK2/STAT3 and contributed to ovarian granulosa cell apoptosis partially through up-regulating NPY2R expression.
[Mh] Termos MeSH primário: Apoptose/genética
Hormônios Esteroides Gonadais/genética
Células da Granulosa/fisiologia
Leptina/metabolismo
Neuropeptídeo Y/metabolismo
Progesterona/biossíntese
Receptores de Neuropeptídeo Y/biossíntese
[Mh] Termos MeSH secundário: Androstenodiona/genética
Animais
Apoptose/efeitos dos fármacos
Arginina/administração & dosagem
Arginina/análogos & derivados
Arginina/farmacologia
Benzazepinas/administração & dosagem
Benzazepinas/farmacologia
Proliferação Celular
Dinoprostona/genética
Feminino
Hormônio Foliculoestimulante/metabolismo
Técnicas de Silenciamento de Genes
Células da Granulosa/citologia
Células da Granulosa/efeitos dos fármacos
Seres Humanos
Janus Quinase 2/biossíntese
Janus Quinase 2/genética
Leptina/genética
Leptina/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Neuropeptídeo Y/antagonistas & inibidores
Progesterona/genética
RNA Interferente Pequeno/metabolismo
Receptores de Neuropeptídeo Y/antagonistas & inibidores
Receptores de Neuropeptídeo Y/genética
Fator de Transcrição STAT3/biossíntese
Fator de Transcrição STAT3/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzazepines); 0 (Gonadal Steroid Hormones); 0 (Leptin); 0 (Neuropeptide Y); 0 (RNA, Small Interfering); 0 (Receptors, Neuropeptide Y); 0 (STAT3 Transcription Factor); 0 (neuropeptide Y2 receptor); 409J2J96VR (Androstenedione); 4G7DS2Q64Y (Progesterone); 9002-68-0 (Follicle Stimulating Hormone); 94ZLA3W45F (Arginine); EC 2.7.10.2 (JAK2 protein, human); EC 2.7.10.2 (Janus Kinase 2); K7Q1JQR04M (Dinoprostone); N3Z657H81X (BIIE 0246)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170903
[St] Status:MEDLINE


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[PMID]:28795803
[Au] Autor:Schubert M; Stichel J; Du Y; Tough IR; Sliwoski G; Meiler J; Cox HM; Weaver CD; Beck-Sickinger AG
[Ad] Endereço:Faculty of Biosciences, Pharmacy and Psychology, Institute of Biochemistry, Leipzig University , Leipzig 04103, Germany.
[Ti] Título:Identification and Characterization of the First Selective Y Receptor Positive Allosteric Modulator.
[So] Source:J Med Chem;60(17):7605-7612, 2017 Sep 14.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The human Y receptor (Y R) and its cognate ligand, pancreatic polypeptide (PP), are involved in the regulation of energy expenditure, satiety, and food intake. This system represents a potential target for the treatment of metabolic diseases and has been extensively investigated and validated in vivo. Here, we present the compound tBPC (tert-butylphenoxycyclohexanol), a novel and selective Y R positive allosteric modulator that potentiates Y R activation in G-protein signaling and arrestin3 recruitment experiments. The compound has no effect on the binding of the orthosteric ligands, implying its allosteric mode of action at the Y R and evidence for a purely efficacy-driven positive allosteric modulation. Finally, the ability of tBPC to selectively potentiate Y R agonism initiated by PP was confirmed in mouse descending colon mucosa preparations expressing native Y R, demonstrating Y R positive allosteric modulation in vitro.
[Mh] Termos MeSH primário: Regulação Alostérica/efeitos dos fármacos
Cicloexanóis/química
Cicloexanóis/farmacologia
Proteínas de Ligação ao GTP/metabolismo
Receptores de Neuropeptídeo Y/agonistas
Receptores de Neuropeptídeo Y/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Arrestinas/metabolismo
Células COS
Cercopithecus aethiops
Células HEK293
Seres Humanos
Modelos Moleculares
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arrestins); 0 (Cyclohexanols); 0 (Receptors, Neuropeptide Y); 0 (arrestin3); 0 (neuropeptide Y4 receptor); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b00976


  5 / 2264 MEDLINE  
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[PMID]:28684122
[Au] Autor:Nishizawa N; Niida A; Adachi Y; Masuda Y; Kumano S; Yokoyama K; Asakawa T; Hirabayashi H; Amano N; Takekawa S; Ohtaki T; Asami T
[Ad] Endereço:Pharmaceutical Research Division, Takeda Pharmaceutical Company, Ltd., Fujisawa 251-8555, Japan.
[Ti] Título:Potent antiobesity effect of a short-length peptide YY-analogue continuously administered in mice.
[So] Source:Bioorg Med Chem Lett;27(16):3829-3832, 2017 08 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The gastrointestinal peptide, peptide YY (PYY ) and its shorter peptide analogues have been reported to reduce appetite by activating the neuropeptide Y2 receptor (Y2R), which is associated with obesity and other metabolic diseases. A 14-amino acid PYY analogue, Ac-[d-Pro ,Cha ,Aib ]PYY(23-36) (3), showed high binding affinity and agonist activity for the Y2R, similar to that of PYY , but had weak anorectic activity upon continuous administration in lean mice. Three amino acid substitutions [Pya(4) , Aib , Lys ], which contributed to the decreased hydrophobicity of 3, efficiently increased its anorectic activity. The compound containing these three amino acids, Ac-[d-Pro ,Pya(4) ,Cha ,Aib ,Lys ]PYY(23-36) (22), exerted more potent and durable food intake suppression than that by PYY in lean mice, as well as excellent Y2R agonist activity (EC : 0.20nM) and good subcutaneous bioavailability (66.6%). The 11-day continuous administration of 22 at 1mg/kg/day successfully produced antiobese and antidiabetic effects, with more than 20% body weight loss in obese and Type 2 diabetes ob/ob model mice.
[Mh] Termos MeSH primário: Fármacos Antiobesidade/farmacologia
Ingestão de Alimentos/efeitos dos fármacos
Obesidade/tratamento farmacológico
Peptídeo YY/farmacologia
[Mh] Termos MeSH secundário: Animais
Fármacos Antiobesidade/administração & dosagem
Fármacos Antiobesidade/química
Relação Dose-Resposta a Droga
Injeções Intravenosas
Injeções Subcutâneas
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Obesos
Estrutura Molecular
Peptídeo YY/administração & dosagem
Peptídeo YY/química
Receptores de Neuropeptídeo Y/agonistas
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Obesity Agents); 0 (Receptors, Neuropeptide Y); 0 (neuropeptide Y2 receptor); 106388-42-5 (Peptide YY)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE


  6 / 2264 MEDLINE  
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[PMID]:28628036
[Au] Autor:Shi Z; Madden CJ; Brooks VL
[Ad] Endereço:Department of Physiology and Pharmacology and.
[Ti] Título:Arcuate neuropeptide Y inhibits sympathetic nerve activity via multiple neuropathways.
[So] Source:J Clin Invest;127(7):2868-2880, 2017 Jun 30.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obesity increases sympathetic nerve activity (SNA) via activation of proopiomelanocortin neurons in the arcuate nucleus (ArcN), and this action requires simultaneous withdrawal of tonic neuropeptide Y (NPY) sympathoinhibition. However, the sites and neurocircuitry by which NPY decreases SNA are unclear. Here, using designer receptors exclusively activated by designer drugs (DREADDs) to selectively activate or inhibit ArcN NPY neurons expressing agouti-related peptide (AgRP) in mice, we have demonstrated that this neuronal population tonically suppresses splanchnic SNA (SSNA), arterial pressure, and heart rate via projections to the paraventricular nucleus (PVN) and dorsomedial hypothalamus (DMH). First, we found that ArcN NPY/AgRP fibers closely appose PVN and DMH presympathetic neurons. Second, nanoinjections of NPY or an NPY receptor Y1 (NPY1R) antagonist into PVN or DMH decreased or increased SSNA, respectively. Third, blockade of DMH NPY1R reversed the sympathoinhibition elicited by selective, DREADD-mediated activation of ArcN NPY/AgRP neurons. Finally, stimulation of ArcN NPY/AgRP terminal fields in the PVN and DMH decreased SSNA. Considering that chronic obesity decreases ArcN NPY content, we propose that the ArcN NPY neuropathway to the PVN and DMH is pivotal in obesity-induced elevations in SNA.
[Mh] Termos MeSH primário: Núcleo Arqueado do Hipotálamo/metabolismo
Pressão Sanguínea
Neuropeptídeo Y/metabolismo
Sistema Nervoso Simpático/metabolismo
Sistema Nervoso Simpático/fisiopatologia
[Mh] Termos MeSH secundário: Proteína Relacionada com Agouti/biossíntese
Proteína Relacionada com Agouti/genética
Animais
Núcleo Arqueado do Hipotálamo/patologia
Núcleo Arqueado do Hipotálamo/fisiopatologia
Doença Crônica
Regulação da Expressão Gênica
Frequência Cardíaca
Camundongos
Camundongos Transgênicos
Neuropeptídeo Y/genética
Obesidade/genética
Obesidade/metabolismo
Obesidade/patologia
Obesidade/fisiopatologia
Núcleo Hipotalâmico Paraventricular/metabolismo
Núcleo Hipotalâmico Paraventricular/patologia
Núcleo Hipotalâmico Paraventricular/fisiopatologia
Receptores de Neuropeptídeo Y/genética
Receptores de Neuropeptídeo Y/metabolismo
Sistema Nervoso Simpático/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Agouti-Related Protein); 0 (Agrp protein, mouse); 0 (Neuropeptide Y); 0 (Npy1r protein, mouse); 0 (Receptors, Neuropeptide Y)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170930
[Lr] Data última revisão:
170930
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE


  7 / 2264 MEDLINE  
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[PMID]:28576472
[Au] Autor:Aubol BE; Hailey KL; Fattet L; Jennings PA; Adams JA
[Ad] Endereço:Department of Pharmacology, University of California, San Diego, La Jolla, CA 92093-0636, USA.
[Ti] Título:Redirecting SR Protein Nuclear Trafficking through an Allosteric Platform.
[So] Source:J Mol Biol;429(14):2178-2191, 2017 Jul 07.
[Is] ISSN:1089-8638
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Although phosphorylation directs serine-arginine (SR) proteins from nuclear storage speckles to the nucleoplasm for splicing function, dephosphorylation paradoxically induces similar movement, raising the question of how such chemical modifications are balanced in these essential splicing factors. In this new study, we investigated the interaction of protein phosphatase 1 (PP1) with the SR protein splicing factor (SRSF1) to understand the foundation of these opposing effects in the nucleus. We found that RNA recognition motif 1 (RRM1) in SRSF1 binds PP1 and represses its catalytic function through an allosteric mechanism. Disruption of RRM1-PP1 interactions reduces the phosphorylation status of the RS domain in vitro and in cells, redirecting SRSF1 in the nucleus. The data imply that an allosteric SR protein-phosphatase platform balances phosphorylation levels in a "goldilocks" region for the proper subnuclear storage of an SR protein splicing factor.
[Mh] Termos MeSH primário: Núcleo Celular/metabolismo
Processamento de Proteína Pós-Traducional
Receptores de Neuropeptídeo Y/metabolismo
Fatores de Processamento de Serina-Arginina/metabolismo
[Mh] Termos MeSH secundário: Regulação Alostérica
Sítios de Ligação
Células HeLa
Seres Humanos
Fosforilação
Ligação Proteica
Conformação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Neuropeptide Y); 0 (SRSF1 protein, human); 0 (neuropeptide Y4 receptor); 170974-22-8 (Serine-Arginine Splicing Factors)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170604
[St] Status:MEDLINE


  8 / 2264 MEDLINE  
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[PMID]:28572154
[Au] Autor:Thangaratnarajah C; Dinger K; Vohlen C; Klaudt C; Nawabi J; Lopez Garcia E; Kwapiszewska G; Dobner J; Nüsken KD; van Koningsbruggen-Rietschel S; von Hörsten S; Dötsch J; Alejandre Alcázar MA
[Ad] Endereço:Translational Experimental Pediatrics, Experimental Pulmonology, University Hospital for Pediatrics and Adolescent Medicine, Faculty of Medicine, University of Cologne, Cologne, Germany.
[Ti] Título:Novel role of NPY in neuroimmune interaction and lung growth after intrauterine growth restriction.
[So] Source:Am J Physiol Lung Cell Mol Physiol;313(3):L491-L506, 2017 Sep 01.
[Is] ISSN:1522-1504
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Individuals with intrauterine growth restriction (IUGR) are at risk for chronic lung disease. Using a rat model, we showed in our previous studies that altered lung structure is related to IL-6/STAT3 signaling. As neuropeptide Y (NPY), a coneurotransmitter of the sympathetic nervous system, regulates proliferation and immune response, we hypothesized that dysregulated NPY after IUGR is linked to IL-6, impaired myofibroblast function, and alveolar growth. IUGR was induced in rats by isocaloric low-protein diet; lungs were analyzed on embryonic day (E) 21, postnatal day (P) 3, P12, and P23. Finally, primary neonatal lung myofibroblasts (pnF) and murine embryonic fibroblasts (MEF) were used to assess proliferation, apoptosis, migration, and IL-6 expression. At E21, NPY and IL-6 expression was decreased, and AKT/PKC and STAT3/AMPKα signaling was reduced. Early reduction of NPY/IL-6 was associated with increased chord length in lungs after IUGR at P3, indicating reduced alveolar formation. At P23, however, IUGR rats exhibited a catch-up of body weight and alveolar growth coupled with more proliferating myofibroblasts. These structural findings after IUGR were linked to activated NPY/PKC, IL-6/AMPKα signaling. Complementary, IUGR-pnF showed increased survival, impaired migration, and reduced IL-6 compared with control-pnF (Co-pnF). In contrast, NPY induced proliferation, migration, and increased IL-6 synthesis in fibroblasts. Additionally, NPY mice showed reduced IL-6 signaling and less proliferation of lung fibroblasts. Our study presents a novel role of NPY during alveolarization: NPY regulates ) IL-6 and lung STAT3/AMPKα signaling, and ) proliferation and migration of myofibroblasts. These new insights in pulmonary neuroimmune interaction offer potential strategies to enable lung growth.
[Mh] Termos MeSH primário: Retardo do Crescimento Fetal/patologia
Pulmão/crescimento & desenvolvimento
Neuropeptídeo Y/metabolismo
Sistema Nervoso Simpático/imunologia
Sistema Nervoso Simpático/patologia
[Mh] Termos MeSH secundário: Adenilato Quinase/metabolismo
Animais
Animais Recém-Nascidos
Apoptose/genética
Biomarcadores/metabolismo
Movimento Celular/genética
Proliferação Celular/genética
Sobrevivência Celular/genética
Dieta
Retardo do Crescimento Fetal/imunologia
Regulação da Expressão Gênica
Interleucina-6/genética
Interleucina-6/metabolismo
Pulmão/patologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
Modelos Biológicos
Miofibroblastos/metabolismo
Neurotransmissores/metabolismo
Proteína Quinase C/metabolismo
Ratos Wistar
Receptores de Neuropeptídeo Y/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais/genética
Proteína 3 Supressora da Sinalização de Citocinas/metabolismo
Ganho de Peso
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Interleukin-6); 0 (Neuropeptide Y); 0 (Neurotransmitter Agents); 0 (Receptors, Neuropeptide Y); 0 (STAT3 Transcription Factor); 0 (Socs3 protein, mouse); 0 (Suppressor of Cytokine Signaling 3 Protein); EC 2.7.11.13 (Protein Kinase C); EC 2.7.4.3 (Adenylate Kinase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1152/ajplung.00432.2016


  9 / 2264 MEDLINE  
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[PMID]:28434803
[Au] Autor:Rouhana L; Tasaki J; Saberi A; Newmark PA
[Ad] Endereço:Department of Biological Sciences, Wright State University, 3640 Colonel Glenn Highway, Dayton, OH 45435, USA; Howard Hughes Medical Institute and Department of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, 601 S. Goodwin Ave., Urbana, IL 61801, USA. Electronic address:
[Ti] Título:Genetic dissection of the planarian reproductive system through characterization of Schmidtea mediterranea CPEB homologs.
[So] Source:Dev Biol;426(1):43-55, 2017 06 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cytoplasmic polyadenylation is a mechanism of mRNA regulation prevalent in metazoan germ cells; it is largely dependent on Cytoplasmic Polyadenylation Element Binding proteins (CPEBs). Two CPEB homologs were identified in the planarian Schmidtea mediterranea. Smed-CPEB1 is expressed in ovaries and yolk glands of sexually mature planarians, and required for oocyte and yolk gland development. In contrast, Smed-CPEB2 is expressed in the testes and the central nervous system; its function is required for spermatogenesis as well as non-autonomously for development of ovaries and accessory reproductive organs. Transcriptome analysis of CPEB knockdown animals uncovered a comprehensive collection of molecular markers for reproductive structures in S. mediterranea, including ovaries, testes, yolk glands, and the copulatory apparatus. Analysis by RNA interference revealed contributions for a dozen of these genes during oogenesis, spermatogenesis, or capsule formation. We also present evidence suggesting that Smed-CPEB2 promotes translation of Neuropeptide Y-8, a prohormone required for planarian sexual maturation. These findings provide mechanistic insight into potentially conserved processes of germ cell development, as well as events involved in capsule deposition by flatworms.
[Mh] Termos MeSH primário: Células Germinativas/citologia
Oogênese/fisiologia
Ovário/crescimento & desenvolvimento
Planárias/anatomia & histologia
Planárias/crescimento & desenvolvimento
Espermatogênese/fisiologia
Fatores de Poliadenilação e Clivagem de mRNA/genética
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/genética
Feminino
Perfilação da Expressão Gênica
Ovário/metabolismo
Poliadenilação
Interferência de RNA
RNA Interferente Pequeno/genética
Receptores de Neuropeptídeo Y/biossíntese
Receptores de Neuropeptídeo Y/genética
Maturidade Sexual/genética
Maturidade Sexual/fisiologia
Fatores de Poliadenilação e Clivagem de mRNA/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (Receptors, Neuropeptide Y); 0 (mRNA Cleavage and Polyadenylation Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE


  10 / 2264 MEDLINE  
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[PMID]:28345900
[Au] Autor:Dukorn S; Littmann T; Keller M; Kuhn K; Cabrele C; Baumeister P; Bernhardt G; Buschauer A
[Ad] Endereço:Institute of Pharmacy, University of Regensburg , Universitätsstraße 31, 93053 Regensburg, Germany.
[Ti] Título:Fluorescence- and Radiolabeling of [Lys ,Nle ]hPP Yields Molecular Tools for the NPY Y Receptor.
[So] Source:Bioconjug Chem;28(4):1291-1304, 2017 Apr 19.
[Is] ISSN:1520-4812
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The neuropeptide Y (NPY) Y receptor (Y R) is involved in energy homeostasis and considered a potential drug target for the treatment of obesity. Only a few molecular tools, i.e., radiolabeled and fluorescent ligands, for the investigation of the Y R were reported. Previously, [Lys ]hPP proved to be an appropriate full-length PP analog to prepare a fluorescent ligand by derivatization at the ε-amino group. To preclude oxidation upon long-term storage, we replaced the two methionine residues in [Lys ]hPP by norleucine and prepared the corresponding [ H]propionylated ([ H]12) and cyanine labeled (13) peptides, which were characterized and compared with a set of reference compounds in binding (Y , Y , Y , and Y receptors) and functional (luciferase gene reporter, beta-arrestin-1,2) Y R assays. Both molecular probes proved to be useful in radiochemical and flow cytometric saturation and competition Y R binding experiments. Most strikingly, there was a different influence of the composition of buffer on equilibrium binding and kinetics: [ H]12 affinity (K in Na -free buffer: 1.1 nM) clearly decreased with increasing sodium ion concentration, whereas dissociation and Y R-mediated internalization of 13 (K in Na -free buffer: 10.8 nM) were strongly affected by the osmolarity of the buffer as demonstrated by confocal microscopy. Displacement of [ H]12 and 13 revealed a tendency to higher apparent affinities for a set of reference peptides in hypotonic (Na -free) compared to isotonic buffers. The differences were negligible in the case of hPP but up to 270-fold in the case of GW1229 (GR231118). By contrast, no relevant influence of Na on Y R affinity became obvious, when the radioligands [H]12 and [ H]propionyl-pNPY were investigated in saturation binding and competition binding.
[Mh] Termos MeSH primário: Sistemas de Liberação de Medicamentos/métodos
Compostos Radiofarmacêuticos/síntese química
Receptores de Neuropeptídeo Y/metabolismo
[Mh] Termos MeSH secundário: Ligação Competitiva
Estabilidade de Medicamentos
Fluorescência
Seres Humanos
Ligantes
Obesidade/tratamento farmacológico
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ligands); 0 (Radiopharmaceuticals); 0 (Receptors, Neuropeptide Y)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE
[do] DOI:10.1021/acs.bioconjchem.7b00103



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