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Pesquisa : D06.472.334.734.769 [Categoria DeCS]
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[PMID]:28453725
[Au] Autor:Nonhoff J; Ricke-Hoch M; Mueller M; Stapel B; Pfeffer T; Kasten M; Scherr M; von Kaisenberg C; Bauersachs J; Haghikia A; Hilfiker-Kleiner D
[Ad] Endereço:Department of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg Str. 1, 30625 Hannover, Germany.
[Ti] Título:Serelaxin treatment promotes adaptive hypertrophy but does not prevent heart failure in experimental peripartum cardiomyopathy.
[So] Source:Cardiovasc Res;113(6):598-608, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: Peripartum cardiomyopathy (PPCM) is a systolic left ventricular dysfunction developing in the peripartum phase in previously healthy women. Relaxin-2 is a pregnancy hormone with potential beneficial effects in heart failure patients. We evaluated Relaxin-2 as a potential diagnostic marker and/or a therapeutic agent in PPCM. Methods and results: In healthy peripartum women, serum Relaxin-2 levels (measured by ELISA in the second half of pregnancy) were elevated showing a decreasing trend in the first postpartum week and returned to non-pregnant levels thereafter. In PPCM patients diagnosed in the first postpartum week, serum Relaxin-2 levels were lower compared to healthy postpartum stage-matched controls. In PPCM patients diagnosed later (0.5-10 months postpartum) Relaxin-2 levels were in the range of non-pregnant controls and not different from healthy postpartum stage-matched controls. In mice, serum Relaxin-1 (functional equivalent of human Relaxin-2) was increased late in pregnancy and rapidly cleared in the first postpartum week. In mice with PPCM due to a cardiomyocyte-specific knockout of STAT3 (CKO) neither low nor high dose of recombinant Relaxin-2 (serelaxin, sRlx-LD: 30 µg/kg/day; sRlx-HD: 300 µg/kg/day) affected cardiac fibrosis, inflammation and heart failure but sRlx-HD increased capillary/cardiomyocyte ratio. sRlx-HD significantly increased heart/body weight ratio and cardiomyocyte cross-sectional area in postpartum CKO and wild-type mice without changing the foetal gene expression program (ANP or ß-MHC). sRlx-HD augmented plasma Prolactin levels in both genotypes, which induced cardiac activation of STAT5. In vitro analyses showed that Prolactin induces cardiomyocyte hypertrophy via activation of STAT5. Conclusion: Although Relaxin-2 levels seemed lower in PPCM patients diagnosed early postpartum, we observed a high pregnancy-related variance of serum Relaxin-2 levels peripartum making it unsuitable as a biomarker for this condition. Supplementation with sRlx may contribute to angiogenesis and compensatory hypertrophy in the diseased heart, but the effects are not sufficient to prevent heart failure in an experimental PPCM model.
[Mh] Termos MeSH primário: Cardiomegalia/patologia
Cardiomiopatias/tratamento farmacológico
Fármacos Cardiovasculares/farmacologia
Insuficiência Cardíaca/prevenção & controle
Miócitos Cardíacos/efeitos dos fármacos
Período Pós-Parto/sangue
Relaxina/farmacologia
[Mh] Termos MeSH secundário: Adulto
Animais
Biomarcadores/sangue
Cardiomegalia/sangue
Cardiomegalia/fisiopatologia
Cardiomiopatias/sangue
Cardiomiopatias/patologia
Cardiomiopatias/fisiopatologia
Estudos de Casos e Controles
Modelos Animais de Doenças
Feminino
Insuficiência Cardíaca/sangue
Insuficiência Cardíaca/patologia
Insuficiência Cardíaca/fisiopatologia
Seres Humanos
Camundongos Knockout
Miócitos Cardíacos/metabolismo
Miócitos Cardíacos/patologia
Gravidez
Prolactina/sangue
Ratos
Proteínas Recombinantes/farmacologia
Sistema de Registros
Relaxina/sangue
Fator de Transcrição STAT3/deficiência
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT5/metabolismo
Transdução de Sinais/efeitos dos fármacos
Volume Sistólico
Função Ventricular Esquerda
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cardiovascular Agents); 0 (RLN2 protein, human); 0 (Recombinant Proteins); 0 (Rln1 protein, mouse); 0 (STAT3 Transcription Factor); 0 (STAT5 Transcription Factor); 0 (Stat3 protein, mouse); 0 (relaxin-3 protein, mouse); 0 (serelaxin protein, human); 9002-62-4 (Prolactin); 9002-69-1 (Relaxin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvw245


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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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[PMID]:29173360
[Au] Autor:Han L; Luo J; Bai S; Jia Y; Chen X; Zhao Y; Chen L; Zhu X; Li Y; Jiang Y; Li X; Yang M; Li D; Teng X; Qi Y
[Ad] Endereço:Department of Cardiology, Fu Xing Hospital, Capital Medical University, Beijing, China.
[Ti] Título:Combined Assessment of Relaxin and B-Type Natriuretic Peptide Improves Diagnostic Value in Patients With Congestive Heart Failure.
[So] Source:Am J Med Sci;354(5):480-485, 2017 11.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: To improve the poor prognosis of congestive heart failure (CHF), early and accurate diagnosis is necessary. Relaxin is an endogenous cardiovascular peptide, and its plasma level is usually increased in patients with CHF. In this pilot study, we aimed to determine the diagnostic value of relaxin and B-type natriuretic peptide (BNP) in patients with and without CHF. MATERIALS AND METHODS: The plasma level of relaxin was measured by enzyme-linked immunosorbent assay and plasma level of BNP by fluorescence immunoassay. The area under the receiver operating characteristic curve was used to assess the diagnostic value of relaxin and BNP. RESULTS: We included 81 patients with decompenstated CHF and 36 controls. Plasma levels of relaxin and BNP were both higher in CHF patients than in controls. The correlation between plasma levels of relaxin and BNP and between relaxin or BNP and cardiac function was nonlinear. Relaxin had medium diagnostic value, and BNP had higher value for cardiac function and CHF. At a cutoff of 39.76pg/mL relaxin, sensitivity was 82.7%, specificity 55.6%, sum of the highest positive predictive value 80.5% and negative predictive value 58.8%. Although the diagnostic value was not better for relaxin than BNP, their combined assessment improved the sensitivity and specificity of diagnosis for CHF as compared with BNP alone. CONCLUSIONS: Combined assessment of relaxin and BNP may improve the diagnosis of decompensated CHF, which may have potential application in the clinic.
[Mh] Termos MeSH primário: Ensaio de Imunoadsorção Enzimática
Fluorimunoensaio
Insuficiência Cardíaca/diagnóstico
Peptídeo Natriurético Encefálico/sangue
Relaxina/sangue
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
China
Feminino
Insuficiência Cardíaca/sangue
Seres Humanos
Masculino
Meia-Idade
Projetos Piloto
Valor Preditivo dos Testes
Curva ROC
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
114471-18-0 (Natriuretic Peptide, Brain); 9002-69-1 (Relaxin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:29346407
[Au] Autor:Martin B; Gabris-Weber BA; Reddy R; Romero G; Chattopadhyay A; Salama G
[Ad] Endereço:Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, United States of America.
[Ti] Título:Relaxin reverses inflammatory and immune signals in aged hearts.
[So] Source:PLoS One;13(1):e0190935, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: 'Healthy' aging drives structural and functional changes in the heart including maladaptive electrical remodeling, fibrosis and inflammation, which lower the threshold for cardiovascular diseases such as heart failure (HF) and atrial fibrillation (AF). Despite mixed results in recent clinical trials, Relaxin-therapy for 2-days could reduce mortality by 37% at 180-days post-treatment, in patients with acute decompensated HF. Relaxin's short life-span (hours) but long-lasting protective actions led us to test the hypothesis that relaxin acts at a genomic level to reverse maladaptive remodeling in aging and HF. METHODS AND RESULTS: Young (9-month) and aged (24-month), male and female F-344/Brown Norway rats were treated with relaxin (0.4 mg/kg/day) for 2-weeks delivered by subcutaneous osmotic mini-pumps or with sodium acetate (controls). The genomic effects of aging and relaxin were evaluated by extracting RNA from the left ventricles and analyzing genomic changes by RNA-sequencing, Ingenuity Pathway Analysis, MetaCore and tissue immunohistochemistry. We found that aging promotes a native inflammatory response with distinct sex-differences and relaxin suppresses transcription of multiple genes and signaling pathways associated with inflammation and HF in both genders. In addition, aging significantly increased: macrophage infiltration and atrial natriuretic peptide levels in female ventricles, and activation of the complement cascade, whereas relaxin reversed these age-related effects. CONCLUSION: These data support the hypothesis that relaxin alters gene transcription and suppresses inflammatory pathways and genes associated with HF and aging. Relaxin's suppression of inflammation and fibrosis supports its potential as a therapy for cardiovascular and inflammation-related diseases, such as HF, AF and diabetes.
[Mh] Termos MeSH primário: Envelhecimento/imunologia
Modelos Animais de Doenças
Coração/efeitos dos fármacos
Inflamação/tratamento farmacológico
Relaxina/uso terapêutico
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Fibrilação Atrial/metabolismo
Biomarcadores/metabolismo
Estudos de Coortes
Feminino
Imunofluorescência
Insuficiência Cardíaca/metabolismo
Seres Humanos
Macrófagos/imunologia
Masculino
Ratos
Ratos Endogâmicos F344
Relaxina/farmacologia
Análise de Sequência de RNA
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 9002-69-1 (Relaxin)
[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:180119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190935


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[PMID]:27774604
[Au] Autor:Ma S; Smith CM; Blasiak A; Gundlach AL
[Ad] Endereço:The Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australia.
[Ti] Título:Distribution, physiology and pharmacology of relaxin-3/RXFP3 systems in brain.
[So] Source:Br J Pharmacol;174(10):1034-1048, 2017 05.
[Is] ISSN:1476-5381
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Relaxin-3 is a member of a superfamily of structurally-related peptides that includes relaxin and insulin-like peptide hormones. Soon after the discovery of the relaxin-3 gene, relaxin-3 was identified as an abundant neuropeptide in brain with a distinctive topographical distribution within a small number of GABAergic neuron populations that is well conserved across species. Relaxin-3 is thought to exert its biological actions through a single class-A GPCR - relaxin-family peptide receptor 3 (RXFP3). Class-A comprises GPCRs for relaxin-3 and insulin-like peptide-5 and other peptides such as orexin and the monoamine transmitters. The RXFP3 receptor is selectively activated by relaxin-3, whereas insulin-like peptide-5 is the cognate ligand for the related RXFP4 receptor. Anatomical and pharmacological evidence obtained over the last decade supports a function of relaxin-3/RXFP3 systems in modulating responses to stress, anxiety-related and motivated behaviours, circadian rhythms, and learning and memory. Electrophysiological studies have identified the ability of RXFP3 agonists to directly hyperpolarise thalamic neurons in vitro, but there are no reports of direct cell signalling effects in vivo. This article provides an overview of earlier studies and highlights more recent research that implicates relaxin-3/RXFP3 neural network signalling in the integration of arousal, motivation, emotion and related cognition, and that has begun to identify the associated neural substrates and mechanisms. Future research directions to better elucidate the connectivity and function of different relaxin-3 neuron populations and their RXFP3-positive target neurons in major experimental species and humans are also identified. LINKED ARTICLES: This article is part of a themed section on Recent Progress in the Understanding of Relaxin Family Peptides and their Receptors. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.10/issuetoc.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
Relaxina/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Receptores Acoplados a Proteínas-G/agonistas
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RLN3 protein, human); 0 (RXFP3 protein, human); 0 (Receptors, G-Protein-Coupled); 9002-69-1 (Relaxin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1111/bph.13659


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[PMID]:28942152
[Au] Autor:Yuan Y; Zhang Y; Han X; Li Y; Zhao X; Sheng L; Li Y
[Ad] Endereço:Department of Cardiology, The First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
[Ti] Título:Relaxin alleviates TGFß1-induced cardiac fibrosis via inhibition of Stat3-dependent autophagy.
[So] Source:Biochem Biophys Res Commun;493(4):1601-1607, 2017 Dec 02.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiac fibrosis is a pathological feature common to a variety of heart diseases such as myocardial infarction, arrhythmias, cardiomyopathies and heart failure. Emerging data has indicted that autophagy is involved in fibrotic synthesis. Relaxin as a pleiotropic hormone can attenuate cardiac fibrosis and hypertrophy, however the exact molecular mechanism remains largely unknown. In this work, we evaluated whether the antifibrotic effect of relaxin relies on regulating autophagy in primary cardiac fibroblasts (CFs). Our results showed that relaxin significantly attenuated TGFß1-induced autophagy in parallel with the reduction of fibrosis. Moreover, relaxin inhibited the phosphorylation of Stat3/Smad3 signaling. Then we observed that knockdown of Stat3 synchronously suppressed the fibrogenesis and autophagic flux which was stimulated by TGFß1 in CFs. More importantly, we simultaneously administrated relaxin and Stat3 knockdown into CFs, which did not cause further downregulation of autophagy process and collagen protein compared with only Stat3 knockdown or relaxin treatment. These data suggested that relaxin ameliorates TGFß-induced fibrosis dependent on Stat3 signaling-mediated autophagy. This study uncovered a previously unrecognized antifibrotic role of relaxin in cardiac fibrosis, which is achieved through the inhibition of Stat3-dependent autophagy, implying a potential therapeutic target in fibrotic diseases.
[Mh] Termos MeSH primário: Cardiomiopatias/patologia
Cardiomiopatias/fisiopatologia
Relaxina/farmacologia
Fator de Transcrição STAT3/antagonistas & inibidores
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Autofagia/efeitos dos fármacos
Autofagia/fisiologia
Cardiomiopatias/tratamento farmacológico
Células Cultivadas
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Fibroblastos/patologia
Fibrose
Técnicas de Silenciamento de Genes
Miocárdio/metabolismo
Miocárdio/patologia
Ratos
Ratos Sprague-Dawley
Relaxina/fisiologia
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (STAT3 Transcription Factor); 0 (Stat3 protein, rat); 0 (Tgfb1 protein, rat); 0 (Transforming Growth Factor beta1); 9002-69-1 (Relaxin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170925
[St] Status:MEDLINE


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[PMID]:28760204
[Au] Autor:Gimpelewicz C; Metra M; Cleland JGF; Szecsödy P; Chang Wun CC; Boer-Martins L; Cotter G; Davison BA; Felker GM; Filippatos G; Greenberg BH; Pang P; Ponikowski P; Severin T; Voors AA; Teerlink JR
[Ad] Endereço:Novartis Pharma AG, Basel, Switzerland. Electronic address: Claudio.gimpelewicz@novartis.com.
[Ti] Título:Effects of serelaxin on the outcome of patients with or without substantial peripheral edema: A subgroup analysis from the RELAX-AHF trial.
[So] Source:Am Heart J;190:113-122, 2017 Aug.
[Is] ISSN:1097-6744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Acute heart failure (AHF) is a heterogeneous disorder, with most of the patients presenting with breathlessness along with varying degrees of peripheral edema. The presence of peripheral edema suggests that volume overload is the cause of decompensation leading to AHF, whereas breathlessness in the absence of edema may reflect a "vascular phenotype." This analysis investigated the characteristics, therapeutic response, and outcome of patients with AHF, with and without overt peripheral edema in the RELAX-AHF trial. METHODS: Physician-assessed edema scores at baseline were used to categorize the population into those with no/mild edema (score 0 or 1+) and moderate/severe edema (score 2+ or 3+). The effect of serelaxin vs placebo was assessed within each subgroup. RESULTS: Patients with moderate/severe edema (n = 583; 50.5%) were more likely to have severe dyspnea, orthopnea (>30°), rales (≥1/3), and elevated jugular venous pressure (>6 cm) than the patients with little or no peripheral edema (n=571; 49.5%). The relative benefits of serelaxin in terms of reduction in breathlessness, lower diuretic requirements, decreased length of initial hospital stay and days in intensive care unit/cardiac care unit, and improved prognosis (180-day cardiovascular and all-cause mortality) were generally similar for patients with or without peripheral edema. However, because patients with moderate/severe peripheral edema had worse outcomes, the absolute benefit was generally greater than in patients with no/mild edema. CONCLUSIONS: Overall, patients with AHF and moderate/severe peripheral edema have a worse prognosis but appear to receive similar relative benefit and perhaps greater absolute benefit from serelaxin administration.
[Mh] Termos MeSH primário: Edema/etiologia
Insuficiência Cardíaca/tratamento farmacológico
Relaxina/administração & dosagem
[Mh] Termos MeSH secundário: Doença Aguda
Idoso
Relação Dose-Resposta a Droga
Edema/tratamento farmacológico
Feminino
Insuficiência Cardíaca/complicações
Seres Humanos
Injeções Intravenosas
Masculino
Proteínas Recombinantes/administração & dosagem
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Recombinant Proteins); 0 (serelaxin protein, human); 9002-69-1 (Relaxin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE


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[PMID]:28634079
[Au] Autor:Beiert T; Tiyerili V; Knappe V; Effelsberg V; Linhart M; Stöckigt F; Klein S; Schierwagen R; Trebicka J; Nickenig G; Schrickel JW; Andrié RP
[Ad] Endereço:Department of Internal Medicine II, University Hospital Bonn, Rheinische Friedrich-Wilhelms University, Bonn, Germany. Electronic address: Thomas.Beiert@ukbonn.de.
[Ti] Título:Relaxin reduces susceptibility to post-infarct atrial fibrillation in mice due to anti-fibrotic and anti-inflammatory properties.
[So] Source:Biochem Biophys Res Commun;490(3):643-649, 2017 Aug 26.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Relaxin-2 (RLX) is a peptide hormone that exerts beneficial anti-fibrotic and anti-inflammatory effects in diverse models of cardiovascular disease. The goal of this study was to determine the effects of RLX treatment on the susceptibility to atrial fibrillation (AF) after myocardial infarction (MI). METHODS: Mice with cryoinfarction of the left anterior ventricular wall were treated for two weeks with either RLX (75 µg/kg/d) or vehicle (sodium acetate) delivered via subcutaneously implanted osmotic minipumps. RESULTS: RLX treatment significantly attenuated the increase in AF-inducibility following cryoinfarction and reduced the mean duration of AF episodes. Furthermore, epicardial mapping of both atria revealed an increase in conduction velocity. In addition to an attenuation of atrial hypertrophy, chronic application of RLX reduced atrial fibrosis, which was linked to a significant reduction in atrial mRNA expression of connective tissue growth factor. Transcript levels of the pro-inflammatory cytokines interleukin-6 and interleukin-1ß were reduced in RLX treated mice, but macrophage infiltration into atrial myocardium was similar in the vehicle and RLX treated groups. CONCLUSION: Treatment with RLX in mice after MI reduces susceptibility to AF due to anti-inflammatory and anti-fibrotic properties. Because to these favorable actions, RLX may become a new therapeutic option in the treatment of AF, even when complicating MI.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Fibrilação Atrial/etiologia
Fibrilação Atrial/prevenção & controle
Átrios do Coração/efeitos dos fármacos
Infarto do Miocárdio/complicações
Relaxina/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/administração & dosagem
Fibrilação Atrial/fisiopatologia
Cardiomegalia/etiologia
Cardiomegalia/fisiopatologia
Cardiomegalia/prevenção & controle
Feminino
Átrios do Coração/fisiopatologia
Masculino
Camundongos
Relaxina/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 9002-69-1 (Relaxin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE


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[PMID]:28606038
[Au] Autor:Garella R; Squecco R; Baccari MC
[Ad] Endereço:Department of Experimental and Clinical Medicine, Section of Physiology, University of Florence, Florence. Italy.
[Ti] Título:Site-related Effects of Relaxin in the Gastrointestinal Tract Through Nitric Oxide Signalling: An Updated Report.
[So] Source:Curr Protein Pept Sci;18(12):1254-1262, 2017.
[Is] ISSN:1875-5550
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The peptide hormone relaxin (RLX), in addition to its effects on reproduction, has been reported to influence gastrointestinal motility. Interestingly, the digestive tract has been shown to express RLX receptors and the hormone appears to exert site-specific effects acting at the neural or at the smooth muscle level, mainly by a nitric oxide (NO)-mediated mechanism. NO, released by the enteric nerves and/or smooth muscle cells, is one of the main mediators of gastrointestinal relaxation. In fact, in murine in vitro preparations, RLX depresses organ motility acting at the neural level in the stomach and at the muscular level in the small intestine; conversely, in the colon, this hormone paradoxically increases contractility operating at both neural and muscle levels. These effects are ascribable to the ability of RLX to selectively regulate the expression of the different nitric oxide synthase (NOS) isoforms in the different gastrointestinal tracts. Furthermore, recent electrophysiological experiments have shown that RLX can directly affect the biophysical properties of ileal and colonic smooth muscle cells. This mini-review is intended to offer an update on the site-related actions of RLX on gastrointestinal tract motility in relation with its site-specific effects on NOS isoforms expression. Based on these properties, RLX might be considered a potential therapeutic approach to gastrointestinal motor dysfunctions related to an altered NO production.
[Mh] Termos MeSH primário: Trato Gastrointestinal/metabolismo
Óxido Nítrico Sintase/genética
Óxido Nítrico/metabolismo
Receptores Acoplados a Proteínas-G/genética
Receptores de Peptídeos/genética
Relaxina/genética
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Motilidade Gastrointestinal/genética
Trato Gastrointestinal/inervação
Regulação da Expressão Gênica
Seres Humanos
Isoenzimas/genética
Isoenzimas/metabolismo
Camundongos
Relaxamento Muscular/fisiologia
Miócitos de Músculo Liso/citologia
Miócitos de Músculo Liso/metabolismo
Óxido Nítrico Sintase/metabolismo
Ratos
Receptores Acoplados a Proteínas-G/metabolismo
Receptores de Peptídeos/metabolismo
Relaxina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Isoenzymes); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Peptide); 0 (Rln1 protein, mouse); 0 (relaxin receptors); 31C4KY9ESH (Nitric Oxide); 9002-69-1 (Relaxin); EC 1.14.13.39 (Nitric Oxide Synthase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE
[do] DOI:10.2174/1389203718666170612104719


  10 / 2138 MEDLINE  
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[PMID]:28416741
[Au] Autor:Chen L; Sha ML; Li D; Zhu YP; Wang XJ; Jiang CY; Xia SJ; Shao Y
[Ad] Endereço:Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
[Ti] Título:Relaxin abrogates renal interstitial fibrosis by regulating macrophage polarization via inhibition of Toll-like receptor 4 signaling.
[So] Source:Oncotarget;8(13):21044-21053, 2017 Mar 28.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Renal fibrosis is a common feature of chronic kidney disease (CKD). To inhibit the CKD process, it is important to prevent renal fibrosis, though CKD remains incurable. Renal fibrosis can be inhibited by relaxin in several experimental models, but the mechanism of relaxin for antifibrotic potential is still not clear. And here we have studied the role of relaxin in macrophage polarization and renal inflammation after unilateral ureteral obstruction (UUO). Our results show that relaxin can downregulate the Toll-like receptor (TLR) 4 signaling, shift macrophage polarization toward the M2 phenotype and ameliorat renal fibrosis in the early stages of UUO. In vitro experiments, it has been confirmed that relaxin can downregulate the TLR4 signaling and induce the M2 macrophage transition. Furthermore, the transitional actions of macrophage phenotype induced by relaxin are significantly blocked by TAK-242, a TLR4 antagonist, in vitro experiments. Thus, there is a novel mechanism of relaxin for antifibrosis that shifts macrophage polarization toward the M2 phenotype via inhibition of TLR4 signaling.
[Mh] Termos MeSH primário: Polaridade Celular/efeitos dos fármacos
Rim/patologia
Macrófagos/efeitos dos fármacos
Relaxina/farmacologia
Insuficiência Renal Crônica/tratamento farmacológico
Insuficiência Renal Crônica/patologia
Receptor 4 Toll-Like/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Modelos Animais de Doenças
Fibrose
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Recombinantes/farmacologia
Proteínas Recombinantes/uso terapêutico
Relaxina/uso terapêutico
Transdução de Sinais
Sulfonamidas/farmacologia
Obstrução Ureteral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RLN2 protein, human); 0 (Recombinant Proteins); 0 (Sulfonamides); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 0 (ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate); 9002-69-1 (Relaxin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170524
[Lr] Data última revisão:
170524
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15483



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