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Pesquisa : D12.776.543.750.750.700 [Categoria DeCS]
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[PMID]:28438614
[Au] Autor:Kovári B; Vranic S; Marchio C; Sapino A; Cserni G
[Ad] Endereço:Department of Pathology, University of Szeged, 6720 Szeged, Hungary. Electronic address: kovari.bence.p@gmail.com.
[Ti] Título:The expression of GHRH and its receptors in breast carcinomas with apocrine differentiation-further evidence of the presence of a GHRH pathway in these tumors.
[So] Source:Hum Pathol;64:164-170, 2017 Jun.
[Is] ISSN:1532-8392
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Apocrine breast carcinomas were evaluated for the expression of components of the growth hormone-releasing hormone (GHRH) autocrine/paracrine pathway: GHRH and its receptors (GHRH-R), as mammary apocrine carcinomas and epithelium seemed to be uniformly positive for GHRH-R in a pilot study. The apocrine phenotype was determined on the basis of hematoxylin-eosin morphology and a congruent immunohistochemical profile (estrogen receptor negativity, androgen receptor and gross cystic disease fluid protein-15 positivity). Thirty-five formalin-fixed, paraffin-embedded apocrine breast cancers in tissue microarrays and 24 cases using whole-tissue sections were evaluated for GHRH-R and GHRH expression by immunohistochemistry using polyclonal antibodies raised against various domains of GHRH-R and one polyclonal antibody specific for GHRH. GHRH-R positivity was detected in the overwhelming majority (ranging from 90% to 100%) of apocrine breast carcinomas with all but one of the antibodies applied. The expression was usually diffuse with only isolated cases showing positivity in less than 50% of tumor cells. With the PA5-33583 antibody, GHRH-R positivity was seen only in 73% of the cases in at least 50% of the tumor cells. GHRH expression was also present in all but one case tested, with more than 50% of the cells expressing it in 30/34 cases. These results support a high rate of GHRH-R and GHRH expression in apocrine breast carcinomas. Whether these findings can be exploited for the targeted treatment of apocrine breast carcinomas with GHRH antagonists requires further study.
[Mh] Termos MeSH primário: Glândulas Apócrinas/química
Biomarcadores Tumorais/análise
Neoplasias da Mama/química
Carcinoma/química
Hormônio Liberador de Hormônio do Crescimento/análise
Receptores de Neuropeptídeos/análise
Receptores de Hormônios Reguladores de Hormônio Hipofisário/análise
[Mh] Termos MeSH secundário: Glândulas Apócrinas/patologia
Biópsia
Neoplasias da Mama/patologia
Carcinoma/patologia
Diferenciação Celular
Feminino
Seres Humanos
Imuno-Histoquímica
Estudos Retrospectivos
Análise Serial de Tecidos
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Receptors, Neuropeptide); 0 (Receptors, Pituitary Hormone-Regulating Hormone); 0 (somatotropin releasing hormone receptor); 9034-39-3 (Growth Hormone-Releasing Hormone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE


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[PMID]:27501283
[Au] Autor:Gregory LC; Alatzoglou KS; McCabe MJ; Hindmarsh PC; Saldanha JW; Romano N; Le Tissier P; Dattani MT
[Ad] Endereço:Section of Genetics and Epigenetics in Health and Disease (L.C.G., K.S.A., M.J.M., P.C.H., M.T.), Genetics and Genomic Medicine Programme, UCL Great Ormond Street Institute of Child Health, London, United Kingdom; Kinghorn Centre for Clinical Genomics (M.J.M.), Garvan Institute of Medical Research,
[Ti] Título:Partial Loss of Function of the GHRH Receptor Leads to Mild Growth Hormone Deficiency.
[So] Source:J Clin Endocrinol Metab;101(10):3608-3615, 2016 Oct.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Recessive mutations in GHRHR are associated with severe isolated growth hormone deficiency (IGHD), with a final height in untreated patients of 130 cm ± 10 cm (-7.2 ± 1.6 SDS; males) and 114 ± 0.7 cm (-8.3 ± 0.1 SDS; females). DESIGN: We hypothesized that a consanguineous Pakistani family with IGHD in three siblings (two males, one female) would have mutations in GH1 or GHRHR. RESULTS: Two novel homozygous missense variants [c.11G>A (p.R4Q), c.236C>T (p.P79L)] at conserved residues were identified in all three siblings. Both were absent from control databases, aside from pR4Q appearing once in heterozygous form in the Exome Aggregation Consortium Browser. The brothers were diagnosed with GH deficiency at 9.8 and 6.0 years (height SDS: -2.24 and -1.23, respectively), with a peak GH of 2.9 µg/liter with low IGF-1/IGF binding protein 3. Their sister presented at 16 years with classic GH deficiency (peak GH <0.1 µg/liter, IGF-1 <3.3 mmol/liter) and attained an untreated near-adult height of 144 cm (-3.0 SDS); the tallest untreated patient with GHRHR mutations reported. An unrelated Pakistani female IGHD patient was also compound homozygous. All patients had a small anterior pituitary on magnetic resonance imaging. Functional analysis revealed a 50% reduction in maximal cAMP response to stimulation with GHRH by the p.R4Q/p.P79L double mutant receptor, with a 100-fold increase in EC50. CONCLUSION: We report the first coexistence of two novel compound homozygous GHRHR variants in two unrelated pedigrees associated with a partial loss of function. Surprisingly, the patients have a relatively mild IGHD phenotype. Analysis revealed that the pP79L mutation is associated with the compromise in function, with the residual partial activity explaining the mild phenotype.
[Mh] Termos MeSH primário: Nanismo Hipofisário/genética
Nanismo Hipofisário/fisiopatologia
Receptores de Neuropeptídeos/genética
Receptores de Hormônios Reguladores de Hormônio Hipofisário/genética
[Mh] Termos MeSH secundário: Adolescente
Criança
Consanguinidade
Feminino
Seres Humanos
Masculino
Mutação de Sentido Incorreto
Paquistão
Linhagem
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Neuropeptide); 0 (Receptors, Pituitary Hormone-Regulating Hormone); 0 (somatotropin releasing hormone receptor)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160809
[St] Status:MEDLINE


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[PMID]:27487365
[Au] Autor:Gruner M; Grubbs J; McDonagh A; Valdes D; Winbush A; van der Linden AM
[Ad] Endereço:Department of Biology, University of Nevada, Reno, Reno, Nevada, United States of America.
[Ti] Título:Cell-Autonomous and Non-Cell-Autonomous Regulation of a Feeding State-Dependent Chemoreceptor Gene via MEF-2 and bHLH Transcription Factors.
[So] Source:PLoS Genet;12(8):e1006237, 2016 Aug.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Food and feeding-state dependent changes in chemoreceptor gene expression may allow Caenorhabditis elegans to modify their chemosensory behavior, but the mechanisms essential for these expression changes remain poorly characterized. We had previously shown that expression of a feeding state-dependent chemoreceptor gene, srh-234, in the ADL sensory neuron of C. elegans is regulated via the MEF-2 transcription factor. Here, we show that MEF-2 acts together with basic helix-loop-helix (bHLH) transcription factors to regulate srh-234 expression as a function of feeding state. We identify a cis-regulatory MEF2 binding site that is necessary and sufficient for the starvation-induced down regulation of srh-234 expression, while an E-box site known to bind bHLH factors is required to drive srh-234 expression in ADL. We show that HLH-2 (E/Daughterless), HLH-3 and HLH-4 (Achaete-scute homologs) act in ADL neurons to regulate srh-234 expression. We further demonstrate that the expression levels of srh-234 in ADL neurons are regulated remotely by MXL-3 (Max-like 3 homolog) and HLH-30 (TFEB ortholog) acting in the intestine, which is dependent on insulin signaling functioning specifically in ADL neurons. We also show that this intestine-to-neuron feeding-state regulation of srh-234 involves a subset of insulin-like peptides. These results combined suggest that chemoreceptor gene expression is regulated by both cell-autonomous and non-cell-autonomous transcriptional mechanisms mediated by MEF2 and bHLH factors, which may allow animals to fine-tune their chemosensory responses in response to changes in their feeding state.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Proteínas de Caenorhabditis elegans/genética
Células Quimiorreceptoras/metabolismo
Receptores de Neuropeptídeos/genética
Receptores de Hormônios Reguladores de Hormônio Hipofisário/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Fatores de Transcrição Hélice-Alça-Hélice Básicos/biossíntese
Sítios de Ligação
Caenorhabditis elegans/genética
Caenorhabditis elegans/crescimento & desenvolvimento
Proteínas de Caenorhabditis elegans/biossíntese
Regulação da Expressão Gênica no Desenvolvimento
Receptores de Neuropeptídeos/biossíntese
Receptores de Hormônios Reguladores de Hormônio Hipofisário/biossíntese
Células Receptoras Sensoriais/metabolismo
Transdução de Sinais/genética
Fatores de Transcrição/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Caenorhabditis elegans Proteins); 0 (HLH-2 protein, C elegans); 0 (HLH-3 protein, C elegans); 0 (MXL-3 protein, C elegans); 0 (Receptors, Neuropeptide); 0 (Receptors, Pituitary Hormone-Regulating Hormone); 0 (Transcription Factors); 0 (mef-2 protein, C elegans); 0 (somatotropin releasing hormone receptor)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170523
[Lr] Data última revisão:
170523
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160804
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006237


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[PMID]:27253996
[Au] Autor:Miletta MC; Petkovic V; Eblé A; Flück CE; Mullis PE
[Ad] Endereço:Division of Pediatric Endocrinology, Diabetology and Metabolism, Department of Pediatrics and Department of Clinical Research, Inselspital, Bern University Hospital, University of Bern, Bern, CH-3010 Switzerland.
[Ti] Título:Rescue of Isolated GH Deficiency Type II (IGHD II) via Pharmacologic Modulation of GH-1 Splicing.
[So] Source:Endocrinology;157(10):3972-3982, 2016 Oct.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Isolated GH deficiency (IGHD) type II, the autosomal dominant form of GHD, is mainly caused by mutations that affect splicing of GH-1. When misspliced RNA is translated, it produces a toxic 17.5-kDa GH isoform that reduces the accumulation and secretion of wild-type-human GH (wt-hGH). Usually, isolated GHD type II patients are treated with daily injections of recombinant human GH in order to maintain normal growth. However, this type of replacement therapy does not prevent toxic effects of the 17.5-kDa GH isoform on the pituitary gland, which can eventually lead to other hormonal deficiencies. Here, we tested the possibility to restore the constitutive splicing pattern of GH-1 by using butyrate, a drug that mainly acts as histone deacetylase inhibitor. To this aim, wt-hGH and/or different hGH-splice site mutants (GH-IVS3+2, GH-IVS3+6, and GH-ISE+28) were transfected in rat pituitary cells expressing human GHRH receptor (GHRHR) (GC-GHRHR). Upon butyrate treatment, GC-GHRHR cells coexpressing wt-hGH and each of the mutants displayed increased GH transcript level, intracellular GH content, and GH secretion when compared with the corresponding untreated condition. The effect of butyrate was most likely mediated by the alternative splicing factor/splicing factor 2. Overexpression of alternative ASF/SF2 in the same experimental setting, indeed, promoted the amount of full-length transcripts thus increasing synthesis and secretion of the 22-kDa GH isoform. In conclusion, our results support the hypothesis that modulation of GH-1 splicing pattern to increase the 22-kDa GH isoform levels can be clinically beneficial and hence a crucial challenge in GHD research.
[Mh] Termos MeSH primário: Butiratos/uso terapêutico
Nanismo Hipofisário/tratamento farmacológico
Hormônio do Crescimento/secreção
Processamento de RNA/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Butiratos/farmacologia
Linhagem Celular
Avaliação Pré-Clínica de Medicamentos
Técnicas de Transferência de Genes
Hormônio do Crescimento/genética
Seres Humanos
Ratos
Receptores de Neuropeptídeos/genética
Receptores de Neuropeptídeos/metabolismo
Receptores de Hormônios Reguladores de Hormônio Hipofisário/genética
Receptores de Hormônios Reguladores de Hormônio Hipofisário/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butyrates); 0 (Receptors, Neuropeptide); 0 (Receptors, Pituitary Hormone-Regulating Hormone); 0 (somatotropin releasing hormone receptor); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170529
[Lr] Data última revisão:
170529
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160603
[St] Status:MEDLINE


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[PMID]:27052215
[Au] Autor:Maliza R; Fujiwara K; Tsukada T; Azuma M; Kikuchi M; Yashiro T
[Ad] Endereço:Division of Histology and Cell Biology, Department of Anatomy, Jichi Medical University School of Medicine, Shimotsuke, Japan.
[Ti] Título:Effects of retinoic acid on growth hormone-releasing hormone receptor, growth hormone secretagogue receptor gene expression and growth hormone secretion in rat anterior pituitary cells.
[So] Source:Endocr J;63(6):555-61, 2016 Jun 30.
[Is] ISSN:1348-4540
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Retinoic acid (RA) is an important signaling molecule in embryonic development and adult tissue. The actions of RA are mediated by the nuclear receptors retinoic acid receptor (RAR) and retinoid X receptor (RXR), which regulate gene expression. RAR and RXR are widely expressed in the anterior pituitary gland. RA was reported to stimulate growth hormone (GH) gene expression in the anterior pituitary cells. However, current evidence is unclear on the role of RA in gene expression of growth hormone-releasing hormone receptor (Ghrh-r), growth hormone secretagogue receptor (Ghs-r) and somatostatin receptors (Sst-rs). Using isolated anterior pituitary cells of rats, we examined the effects of RA on gene expression of these receptors and GH release. Quantitative real-time PCR revealed that treatment with all-trans retinoic acid (ATRA; 10(-6) M) for 24 h increased gene expression levels of Ghrh-r and Ghs-r; however, expressions of Sst-r2 and Sst-r5 were unchanged. Combination treatment with the RAR-agonist Am80 and RXR-agonist PA024 mimicked the effects of ATRA on Ghrh-r and Ghs-r gene expressions. Exposure of isolated pituitary cells to ATRA had no effect on basal GH release. In contrast, ATRA increased growth hormone-releasing hormone (GHRH)- and ghrelin-stimulated GH release from cultured anterior pituitary cells. Our results suggest that expressions of Ghrh-r and Ghs-r are regulated by RA through the RAR-RXR receptor complex and that RA enhances the effects of GHRH and ghrelin on GH release from the anterior pituitary gland.
[Mh] Termos MeSH primário: Hormônio do Crescimento/secreção
Adeno-Hipófise/efeitos dos fármacos
Adeno-Hipófise/metabolismo
Receptores de Grelina/genética
Receptores de Neuropeptídeos/genética
Receptores de Hormônios Reguladores de Hormônio Hipofisário/genética
Tretinoína/farmacologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Relação Dose-Resposta a Droga
Regulação da Expressão Gênica/efeitos dos fármacos
Masculino
Ratos
Ratos Wistar
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Ghrelin); 0 (Receptors, Neuropeptide); 0 (Receptors, Pituitary Hormone-Regulating Hormone); 0 (somatotropin releasing hormone receptor); 5688UTC01R (Tretinoin); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170303
[Lr] Data última revisão:
170303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160408
[St] Status:MEDLINE
[do] DOI:10.1507/endocrj.EJ16-0086


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[PMID]:27031974
[Au] Autor:de Silva KS; Tennekoon KH; Sundralingam T; Navarathne B; Hewage AS; de Silva WS; Ganihigama D; Jayasinghe HD; Muhandiram ME
[Ad] Endereço:Department of Paediatrics, Faculty of Medicine, University of Colombo, Sri Lanka. shamyadesilva@hotmail.com.
[Ti] Título:Growth hormone releasing hormone receptor codon 72 mutation in a cohort of Sri Lankan patients with growth hormone deficiency.
[So] Source:Ceylon Med J;61(1):18-21, 2016 Mar.
[Is] ISSN:0009-0875
[Cp] País de publicação:Sri Lanka
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Growth hormone releasing hormone receptor (GHRH-R) codon 72 mutation is recognised as a common genetic cause of growth hormone deficiency (GHD) in the Indian subcontinent resulting in a characteristic lean phenotype. Genetic studies have not been previously carried out in Sri Lankans with GHD. METHODS: Patients with GHD presenting to a tertiary care referral centre were studied for GHRH-R codon 72 mutation by PCR amplification and sequencing. The phenotype of the cohort was described as the BMI SDS (Body mass index standard deviation score) based on the anthropometric data at the time of diagnosis. RESULTS: Among 91 patients from 88 families studied, eight (6 boys) carried the codon 72 mutation. The presence of this mutation was low among the Sinhalese ethnicity (3 out of 68) than among Tamil and Moor ethnicities. BMI SDS of <-2 was seen in 71% of mutation positive and 45.8% of mutation negative patients. CONCLUSIONS: Prevalence of GHRH-R codon 72 mutation in this group of GH deficient patients was 8.8%. The lean phenotype observed in 71% of the mutation positive patients was not a significant association when compared to a similar phenotype in 45.8% of the mutation negative patients.
[Mh] Termos MeSH primário: Índice de Massa Corporal
Hormônio do Crescimento/deficiência
Receptores de Neuropeptídeos/genética
Receptores de Hormônios Reguladores de Hormônio Hipofisário/genética
Magreza/genética
[Mh] Termos MeSH secundário: Adolescente
Criança
Pré-Escolar
Códon
Estudos de Coortes
Feminino
Seres Humanos
Masculino
Mutação
Fenótipo
Sri Lanka
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Codon); 0 (Receptors, Neuropeptide); 0 (Receptors, Pituitary Hormone-Regulating Hormone); 0 (somatotropin releasing hormone receptor); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170202
[Lr] Data última revisão:
170202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160401
[St] Status:MEDLINE
[do] DOI:10.4038/cmj.v61i1.8257


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[PMID]:26917260
[Au] Autor:Liu AX; Zhang D; Zhu YM; Gao HJ; Jiang JY; Hu XL; Lv PP; Leung PC; Huang HF
[Ti] Título:Impact of Axis of GHRH and GHRH Receptor on Cell Viability and Apoptosis of the Placental Choriocarcinoma Cell Line.
[So] Source:Curr Mol Med;16(3):299-311, 2016.
[Is] ISSN:1875-5666
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Although GHRH and GHRH-R are recognized as key factors in placental development, little is known about the mechanism(s) of the regulation in trophoblastic cells during placental development. The objective of this study is to determine the potential relationship between the expression levels of GHRH-R and the placental and JEG-3 cell function. Furthermore, we aim to investigate the downstream pathways of GHRH/GHRH-R axis in the control of the JEG-3 cell viability and apoptosis. In this study, we detected the expression pattern of GHRH-R in human chorionic villous tissues and JEG-3 cell. Then, we evaluated the effects of GHRH/GHRH-R and the downstream pathways by using GHRH antagonist (JMR-132) on JEG-3 cell. Our present study found the expressions of GHRH-R in placental villous tissues and JEG-3 cell, and the expression levels of GHRH-R was significantly lower in villous tissues of early pregnancy loss when compared to normal controls. JMR-132 inhibited cellular viability and induced apoptosis in JEG-3 cell in a time and dosedependent manners through activation of caspase-3, p38, and p53, as well as inhibition of phosphorylation of Akt. Interestingly, ER stress markers such as GRP78, ubiquitinated proteins and phospho-eIF2α were significantly increased in JEG-3 cell after being treated with JMR-132. Conversely, pretreated with salubrinal (a selective inhibition of protein phosphatase 1-mediated eIF2α dephosphorylation), JEG-3 cells were rescued from JMR-132-mediated cell growth inhibition, and abolished JMR-132-induced cleaved caspase-3, CHOP, phospho-p53, and ubiquitinated proteins accumulation. Knockdown of endogenous GHRH-R significantly abolished the JMR-132-induced cleaved caspase-3 and activation of p38. In conclusion, our results, for the first time, demonstrated the expression levels of GHRH-R were closely related to the placental function. Inhibition of GHRH-R by using GHRH antagonist in JEG-3 cell may reduce cell viability and induce apoptosis through inactivation of Akt and ER stress via phosphorylation of eIF2α. These observations have enriched our understanding on the function of GHRH/GHRH-R axis and the downstream pathways in the control of the placental development. The Most Important Aspect of the Paper: Our present study for the first time provided evidences that GHRH and GHRH-R loops involve in JEG-3 cell viability and apoptosis through Akt and eIF2α pathways.
[Mh] Termos MeSH primário: Vilosidades Coriônicas/metabolismo
Fator de Iniciação 2 em Eucariotos/genética
Hormônio Liberador de Hormônio do Crescimento/genética
Proteínas Proto-Oncogênicas c-akt/genética
Receptores de Neuropeptídeos/genética
Receptores de Hormônios Reguladores de Hormônio Hipofisário/genética
Trofoblastos/metabolismo
[Mh] Termos MeSH secundário: Aborto Espontâneo/genética
Aborto Espontâneo/metabolismo
Aborto Espontâneo/patologia
Adulto
Apoptose
Estudos de Casos e Controles
Caspase 3/genética
Caspase 3/metabolismo
Linhagem Celular Tumoral
Sobrevivência Celular
Vilosidades Coriônicas/efeitos dos fármacos
Vilosidades Coriônicas/patologia
Cinamatos/farmacologia
Fator de Iniciação 2 em Eucariotos/metabolismo
Feminino
Regulação da Expressão Gênica
Hormônio Liberador de Hormônio do Crescimento/metabolismo
Seres Humanos
Gravidez
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores de Neuropeptídeos/metabolismo
Receptores de Hormônios Reguladores de Hormônio Hipofisário/metabolismo
Sermorelina/análogos & derivados
Sermorelina/antagonistas & inibidores
Sermorelina/farmacologia
Transdução de Sinais
Tioureia/análogos & derivados
Tioureia/farmacologia
Trofoblastos/efeitos dos fármacos
Trofoblastos/patologia
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/genética
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cinnamates); 0 (Eukaryotic Initiation Factor-2); 0 (GHRH(1-29)NH2, PhAcTyr(1)-Arg(2)-P(H)e(4-CL)(6)-Ala(8)-Tyr(Me)(10)-His(11)-Abu(15)-His(20)-Nle(27)-Arg(28)-HLCr(29)-); 0 (Receptors, Neuropeptide); 0 (Receptors, Pituitary Hormone-Regulating Hormone); 0 (Tumor Suppressor Protein p53); 0 (salubrinal); 0 (somatotropin releasing hormone receptor); 86168-78-7 (Sermorelin); 9034-39-3 (Growth Hormone-Releasing Hormone); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3); GYV9AM2QAG (Thiourea)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160227
[St] Status:MEDLINE


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[PMID]:26868211
[Au] Autor:Ma Q; Xia X; Tao Q; Lu K; Shen J; Xu Q; Hu X; Tang Y; Block NL; Webster KA; Schally AV; Wang J; Yu H
[Ti] Título:Profound Actions of an Agonist of Growth Hormone-Releasing Hormone on Angiogenic Therapy by Mesenchymal Stem Cells.
[So] Source:Arterioscler Thromb Vasc Biol;36(4):663-672, 2016 Apr.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The efficiency of cell therapy is limited by poor cell survival and engraftment. Here, we studied the effect of the growth hormone-releasing hormone agonist, JI-34, on mesenchymal stem cell (MSC) survival and angiogenic therapy in a mouse model of critical limb ischemia. APPROACH AND RESULTS: Mouse bone marrow-derived MSCs were incubated with or without 10(-8) mol/L JI-34 for 24 hours. MSCs were then exposed to hypoxia and serum deprivation to detect the effect of preconditioning on cell apoptosis, migration, and tube formation. For in vivo tests, critical limb ischemia was induced by femoral artery ligation. After surgery, mice received 50 µL phosphate-buffered saline or with 1×10(6) MSCs or with 1×10(6) JI-34-reconditioned MSCs. Treatment of MSCs with JI-34 improved MSC viability and mobility and markedly enhanced their capability to promote endothelial tube formation in vitro. These effects were paralleled by an increased phosphorylation and nuclear translocation of signal transducer and activator of transcription 3. In vivo, JI-34 pretreatment enhanced the engraftment of MSCs into ischemic hindlimb muscles and augmented reperfusion and limb salvage compared with untreated MSCs. Significantly more vasculature and proliferating CD31(+) and CD34(+) cells were detected in ischemic muscles that received MSCs treated with JI-34. CONCLUSIONS: Our studies demonstrate a novel role for JI-34 to markedly improve therapeutic angiogenesis in hindlimb ischemia by increasing the viability and mobility of MSCs. These findings support additional studies to explore the full potential of growth hormone-releasing hormone agonists to augment cell therapy in the management of ischemia.
[Mh] Termos MeSH primário: Hormônio Liberador de Hormônio do Crescimento/análogos & derivados
Hormônio Liberador de Hormônio do Crescimento/agonistas
Isquemia/terapia
Transplante de Células-Tronco Mesenquimais
Células Mesenquimais Estromais/efeitos dos fármacos
Músculo Esquelético/irrigação sanguínea
Fragmentos de Peptídeos/farmacologia
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular
Animais
Antígenos CD34/metabolismo
Apoptose/efeitos dos fármacos
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Feminino
Hormônio Liberador de Hormônio do Crescimento/metabolismo
Hormônio Liberador de Hormônio do Crescimento/farmacologia
Membro Posterior
Isquemia/metabolismo
Isquemia/fisiopatologia
Masculino
Células Mesenquimais Estromais/metabolismo
Camundongos Endogâmicos C57BL
Neovascularização Fisiológica
Fosforilação
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Receptores de Neuropeptídeos/agonistas
Receptores de Neuropeptídeos/metabolismo
Receptores de Hormônios Reguladores de Hormônio Hipofisário/agonistas
Receptores de Hormônios Reguladores de Hormônio Hipofisário/metabolismo
Fator de Transcrição STAT3/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (GH-RH(1-29), desaminotyrosyl(1)-ornithyl(12,21)-alpha-aminobutryic acid(15)-norleucyl(27)-aspartyl(28)-agmatine(29)-); 0 (Peptide Fragments); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Receptors, Neuropeptide); 0 (Receptors, Pituitary Hormone-Regulating Hormone); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (somatotropin releasing hormone receptor); 9034-39-3 (Growth Hormone-Releasing Hormone)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160213
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.116.307126


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[PMID]:26831066
[Au] Autor:Romero MJ; Lucas R; Dou H; Sridhar S; Czikora I; Mosieri EM; Rick FG; Block NL; Sridhar S; Fulton D; Weintraub NL; Bagi Z; Schally AV
[Ad] Endereço:Vascular Biology Center, Medical College of Georgia, Augusta University, Augusta, GA 30912; Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, Augusta, GA 30912; Department of Anesthesiology and Perioperative Medicine, Medical College of Georgia, Augusta Unive
[Ti] Título:Role of growth hormone-releasing hormone in dyslipidemia associated with experimental type 1 diabetes.
[So] Source:Proc Natl Acad Sci U S A;113(7):1895-900, 2016 Feb 16.
[Is] ISSN:1091-6490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dyslipidemia associated with triglyceride-rich lipoproteins (TRLs) represents an important residual risk factor for cardiovascular and chronic kidney disease in patients with type 1 diabetes (T1D). Levels of growth hormone (GH) are elevated in T1D, which aggravates both hyperglycemia and dyslipidemia. The hypothalamic growth hormone-releasing hormone (GHRH) regulates the release of GH by the pituitary but also exerts separate actions on peripheral GHRH receptors, the functional role of which remains elusive in T1D. In a rat model of streptozotocin (STZ)-induced T1D, GHRH receptor expression was found to be up-regulated in the distal small intestine, a tissue involved in chylomicron synthesis. Treatment of T1D rats with a GHRH antagonist, MIA-602, at a dose that did not affect plasma GH levels, significantly reduced TRL, as well as markers of renal injury, and improved endothelial-dependent vasorelaxation. Glucagon-like peptide 1 (GLP-1) reduces hyperglucagonemia and postprandial TRL, the latter in part through a decreased synthesis of apolipoprotein B-48 (ApoB-48) by intestinal cells. Although plasma GLP-1 levels were elevated in diabetic animals, this was accompanied by increased rather than reduced glucagon levels, suggesting impaired GLP-1 signaling. Treatment with MIA-602 normalized GLP-1 and glucagon to control levels in T1D rats. MIA-602 also decreased secretion of ApoB-48 from rat intestinal epithelial cells in response to oleic acid stimulation in vitro, in part through a GLP-1-dependent mechanism. Our findings support the hypothesis that antagonizing the signaling of GHRH in T1D may improve GLP-1 function in the small intestine, which, in turn, diminishes TRL and reduces renal and vascular complications.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/fisiopatologia
Modelos Animais de Doenças
Dislipidemias/fisiopatologia
Hormônio Liberador de Hormônio do Crescimento/fisiologia
[Mh] Termos MeSH secundário: Animais
Dislipidemias/terapia
Hormônio Liberador de Hormônio do Crescimento/antagonistas & inibidores
Intestino Delgado/metabolismo
Masculino
Ratos
Ratos Wistar
Receptores de Neuropeptídeos/metabolismo
Receptores de Hormônios Reguladores de Hormônio Hipofisário/metabolismo
Estreptozocina
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Receptors, Neuropeptide); 0 (Receptors, Pituitary Hormone-Regulating Hormone); 0 (somatotropin releasing hormone receptor); 5W494URQ81 (Streptozocin); 9034-39-3 (Growth Hormone-Releasing Hormone)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160203
[St] Status:MEDLINE
[do] DOI:10.1073/pnas.1525520113


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Texto completo
[PMID]:26774398
[Au] Autor:Higuti E; Cecchi CR; Oliveira NA; Lima ER; Vieira DP; Aagaard L; Jensen TG; Jorge AA; Bartolini P; Peroni CN
[Ad] Endereço:Biotechnology Center, Instituto de Pesquisas Energéticas e Nucleares (IPEN-CNEN), Cidade Universitária, São Paulo, SP, Brazil.
[Ti] Título:Partial correction of the dwarf phenotype by non-viral transfer of the growth hormone gene in mice: Treatment age is critical.
[So] Source:Growth Horm IGF Res;26:1-7, 2016 Feb.
[Is] ISSN:1532-2238
[Cp] País de publicação:Scotland
[La] Idioma:eng
[Ab] Resumo:Non-viral transfer of the growth hormone gene to different muscles of immunodeficient dwarf (lit/scid) mice is under study with the objective of improving phenotypic correction via this particular gene therapy approach. Plasmid DNA was administered into the exposed quadriceps or non-exposed tibialis cranialis muscle of lit/scid mice followed by electroporation, monitoring several growth parameters. In a 6-month bioassay, 50µg DNA were injected three times into the quadriceps muscle of 80-day old mice. A 50% weight increase, with a catch-up growth of 21%, together with a 16% increase for nose-to-tail and tail lengths (catch-up=19-21%) and a 24-28% increase for femur length (catch-up=53-60%), were obtained. mIGF1 serum levels were ~7-fold higher than the basal levels for untreated mice, but still ~2-fold lower than in non-dwarf scid mice. Since treatment age was found to be particularly important in a second bioassay utilizing 40-day old mice, these pubertal mice were compared in a third bioassay with adult (80-day old) mice, all treated twice with 50µg DNA injected into each tibialis cranialis muscle, via a less invasive approach. mIGF1 concentrations at the same level as co-aged scid mice were obtained 15days after administration in pubertal mice. Catch-up growth, based on femur length (77%), nose-to-tail (36%) and tail length (39%) increases was 40 to 95% higher than those obtained upon treating adult mice. These data pave the way for the development of more effective pre-clinical assays in pubertal dwarf mice for the treatment of GH deficiency via plasmid-DNA muscular administration.
[Mh] Termos MeSH primário: Nanismo/genética
Técnicas de Transferência de Genes
Terapia Genética/métodos
Hormônio do Crescimento/genética
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Feminino
Crescimento/genética
Crescimento/fisiologia
Hormônio do Crescimento/administração & dosagem
Injeções Intramusculares
Camundongos
Camundongos Endogâmicos C57BL
Camundongos SCID
Fenótipo
Receptores de Neuropeptídeos/genética
Receptores de Hormônios Reguladores de Hormônio Hipofisário/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Neuropeptide); 0 (Receptors, Pituitary Hormone-Regulating Hormone); 0 (somatotropin releasing hormone receptor); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160118
[St] Status:MEDLINE



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