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Pesquisa : A07.541.704.570 [Categoria DeCS]
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[PMID]:29382818
[Au] Autor:Sánchez-Iranzo H; Galardi-Castilla M; Minguillón C; Sanz-Morejón A; González-Rosa JM; Felker A; Ernst A; Guzmán-Martínez G; Mosimann C; Mercader N
[Ad] Endereço:Development of the Epicardium and Its Role during Regeneration Group, Centro Nacional de Investigaciones Cardiovasculares (CNIC-ISCIII), Melchor Fernández Almagro 3, 28029, Madrid, Spain.
[Ti] Título:Tbx5a lineage tracing shows cardiomyocyte plasticity during zebrafish heart regeneration.
[So] Source:Nat Commun;9(1):428, 2018 01 30.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:During development, mesodermal progenitors from the first heart field (FHF) form a primitive cardiac tube, to which progenitors from the second heart field (SHF) are added. The contribution of FHF and SHF progenitors to the adult zebrafish heart has not been studied to date. Here we find, using genetic tbx5a lineage tracing tools, that the ventricular myocardium in the adult zebrafish is mainly derived from tbx5a cells, with a small contribution from tbx5a SHF progenitors. Notably, ablation of ventricular tbx5a -derived cardiomyocytes in the embryo is compensated by expansion of SHF-derived cells. In the adult, tbx5a expression is restricted to the trabeculae and excluded from the outer cortical layer. tbx5a-lineage tracing revealed that trabecular cardiomyocytes can switch their fate and differentiate into cortical myocardium during adult heart regeneration. We conclude that a high degree of cardiomyocyte cell fate plasticity contributes to efficient regeneration.
[Mh] Termos MeSH primário: Ventrículos do Coração/citologia
Miocárdio/citologia
Miócitos Cardíacos/citologia
Regeneração/genética
Proteínas com Domínio T-Box/genética
Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Diferenciação Celular
Linhagem da Célula/genética
Rastreamento de Células
Embrião não Mamífero
Regulação da Expressão Gênica no Desenvolvimento
Genes Reporter
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Ventrículos do Coração/crescimento & desenvolvimento
Ventrículos do Coração/metabolismo
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Miocárdio/metabolismo
Miócitos Cardíacos/metabolismo
Cadeias Leves de Miosina/genética
Cadeias Leves de Miosina/metabolismo
Organogênese/genética
Células-Tronco/citologia
Células-Tronco/metabolismo
Proteínas com Domínio T-Box/deficiência
Peixe-Zebra/crescimento & desenvolvimento
Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Luminescent Proteins); 0 (Myosin Light Chains); 0 (T-Box Domain Proteins); 0 (T-box transcription factor 5); 0 (red fluorescent protein); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02650-6


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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]:29374923
[Au] Autor:Bai XZ; He T; Zhang JL; Liu Y; Cao MY; Zhang JN; Cai WX; Jia YH; Shi JH; Su LL; Hu DH
[Ad] Endereço:Burn Center of PLA, Department of Burns and Cutaneous Surgery, Xijing Hospital, Air Force Medical University, Xi'an 710032, China.
[Ti] Título:[Effects of microRNA-34a on regulating silent information regulator 1 and influence of the factor on myocardial damage of rats with severe burns at early stage].
[So] Source:Zhonghua Shao Shang Za Zhi;34(1):21-28, 2018 Jan 20.
[Is] ISSN:1009-2587
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To explore the effects of microRNA-34a on regulating silent information regulator 1 (SIRT1) and influence of SIRT1 on myocardial damage of rats with severe burns at early stage. (1) Twenty-four Sprague-Dawley (SD) rats were divided into sham injury (SI) group, simple burns (SB) group and SIRT1 agonist (SA) group according to the random number table (the same grouping method below), with 8 rats in each group. Rats in groups SB and SA were inflicted with 30% total body surface area full-thickness scald (hereinafter referred to as burns) on the back, and rats in group SI were sham injuried on the back. Immediately after injury, rats in groups SI and SB were intraperitoneally injected with normal saline of 50 mL/kg, and rats in group SA were intraperitoneally injected with normal saline of 50 mL/kg and 1 mg/mL resveratrol of 50 mg/kg. At 6 h post injury, abdominal aortic blood was collected to make serum and myocardial tissue of rats was collected. (2) Myocardial cells of twelve neonatal SD rats were collected and divided into microRNA-34a mimic control (MMC) group, microRNA-34a mimic (MM) group, microRNA-34a inhibitor control (MIC) group, and microRNA-34a inhibitor (MI) group, which were respectively transfected with gene sequences of mimic control, mimic, inhibitor control, and inhibitor of microRNA-34a. The microRNA-34a expression level and protein expression level of SIRT1 in myocardial cells were respectively detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. Another batch of myocardial cells were divided into microRNA-34a inhibitor control+ burn serum (MCB) group, microRNA-34a inhibitor+ burn serum (MB) group, and microRNA-34a inhibitor+ burn serum + EX527 (MBE) group. Myocardial cells in group MCB were transfected with gene sequence of inhibitor control, and myocardial cells in the later groups were transfected with gene sequence of inhibitor of microRNA-34a. After transfection of 48 h, myocardial cells in group MBE were cultured in Dulbecco's modified Eagle's medium (DMEM) solution for 6 hours, with serum in group SB of volume fraction of 10% and final amount-of-substance concentration of 1 mol/L, and myocardial cells in the other 2 groups were cultured in DMEM solution with serum from rats of group SB of volume fraction of 10%. The protein expression levels of myocardial cells of SIRT1, cleaved-caspase-3, and Bax were detected by Western blotting. (3) Myocardial tissue from (1) was collected to detect expression levels of microRNA-34a and mRNA of SIRT1 in groups SI and SB by real-time fluorescence quantitative RT-PCR. Morphology of myocardial tissue of rats in groups SI, SB, and SA was observed with biological image navigator. The mRNA expression levels of interleukin 1ß (IL-1ß) and tumor necrosis factor (TNF-α) of rats in groups SI, SB, and SA were detected by real-time fluorescence quantitative RT-PCR. The expression levels of cleaved-caspase-3, and Bax of myocardial tissue of rats in groups SI, SB, and SA were detected by Western blotting. Data were processed with one-way analysis of variance and least-significant difference test. (1) After transfection of 48 h, the expression level of microRNA-34a of myocardial cells in group MM was 4.67±0.92, significantly higher than 1.03±0.04 in group MMC ( <0.01); the protein expression level of SIRT1 of myocardial cells in group MM was 0.35±0.06, significantly lower than 1.12±0.11 in group MMC ( <0.01). After transfection of 48 h, the expression level of microRNA-34a of myocardial cells in group MI was 0.26±0.07, significantly lower than 1.33±0.07 in group MIC ( <0.01); the protein expression level of SIRT1 of myocardial cells in group MIC was 1.12±0.16, significantly lower than 1.74±0.34 in group MI ( <0.01). At 6 h after culture, compared with those in group MCB, the SIRT1 protein expression level of myocardial cells in group MB was significantly increased ( <0.05), while cleaved-caspase-3 and Bax protein expression levels of myocardial cells in group MB were significantly decreased ( <0.05). Compared with those in group MB, the SIRT1 protein expression level of myocardial cells in group MBE was with no significantly statistical difference ( >0.05), and cleaved-caspase-3 and Bax protein expression levels were significantly increased ( <0.05). (2) At 6 h post injury, compared with that in group SI, the microRNA-34a expression level of myocardial tissue in group SB was significantly increased ( <0.01), and the mRNA expression level of SIRT1 of myocardial tissue in group SB was significantly decreased ( <0.01). At 6 h post injury, myocardial cells in group SI arranged neatly with normal nucleus and no inflammatory cells infiltration; myocardial cells in group SB arranged disorderly, with no abnormal nucleus, and obvious inflammatory cells infiltration; myocardial cells in group SA arranged neatly, with normal nucleus and little inflammatory cells infiltration. At 6 h post injury, compared with those in group SB, the mRNA expression levels of IL-1ß and TNF-α, and the protein expression levels of cleaved-caspase-3 and Bax of myocardial tissue in groups SI and SA were significantly decreased ( <0.01). The microRNA-34a expression level of myocardial tissue of rats with severe burns at early stage increases, which decreases the expression level of SIRT1, and increases the expression levels of IL-1ß, TNF-α, cleaved-caspase-3 and Bax, leading to obvious myocardial damage. Activation of SIRT1 can alleviate myocardial damage of rats with severe burns at early stage through decreasing expression levels of IL-1ß, TNF-α, cleaved-caspase-3, and Bax.
[Mh] Termos MeSH primário: Queimaduras
MicroRNAs/genética
Miocárdio/metabolismo
Sirtuína 1/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Caspase 3/genética
Caspase 3/metabolismo
Interleucina-1beta
Miocárdio/patologia
Miócitos Cardíacos
RNA Mensageiro/genética
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
Sirtuína 1/genética
Estilbenos
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (MicroRNAs); 0 (RNA, Messenger); 0 (Stilbenes); 0 (Tumor Necrosis Factor-alpha); EC 3.4.22.- (Caspase 3); EC 3.5.1.- (Sirt1 protein, rat); EC 3.5.1.- (Sirtuin 1); Q369O8926L (resveratrol)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1009-2587.2018.01.005


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[PMID]:29295976
[Au] Autor:Liu CY; Zhang YH; Li RB; Zhou LY; An T; Zhang RC; Zhai M; Huang Y; Yan KW; Dong YH; Ponnusamy M; Shan C; Xu S; Wang Q; Zhang YH; Zhang J; Wang K
[Ad] Endereço:Center for Developmental Cardiology, Institute for Translational Medicine, College of Medicine, Qingdao University, Qingdao, 266021, China.
[Ti] Título:LncRNA CAIF inhibits autophagy and attenuates myocardial infarction by blocking p53-mediated myocardin transcription.
[So] Source:Nat Commun;9(1):29, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Increasing evidence suggests that long noncoding RNAs (lncRNAs) play crucial roles in various biological processes. However, little is known about the effects of lncRNAs on autophagy. Here we report that a lncRNA, termed cardiac autophagy inhibitory factor (CAIF), suppresses cardiac autophagy and attenuates myocardial infarction by targeting p53-mediated myocardin transcription. Myocardin expression is upregulated upon H O and ischemia/reperfusion, and knockdown of myocardin inhibits autophagy and attenuates myocardial infarction. p53 regulates cardiomyocytes autophagy and myocardial ischemia/reperfusion injury by regulating myocardin expression. CAIF directly binds to p53 protein and blocks p53-mediated myocardin transcription, which results in the decrease of myocardin expression. Collectively, our data reveal a novel CAIF-p53-myocardin axis as a critical regulator in cardiomyocyte autophagy, which will be potential therapeutic targets in treatment of defective autophagy-associated cardiovascular diseases.
[Mh] Termos MeSH primário: Autofagia/genética
Infarto do Miocárdio/genética
Proteínas Nucleares/genética
RNA Longo não Codificante/genética
Transativadores/genética
Ativação Transcricional
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Células Cultivadas
Camundongos
Infarto do Miocárdio/patologia
Traumatismo por Reperfusão Miocárdica/genética
Traumatismo por Reperfusão Miocárdica/metabolismo
Miócitos Cardíacos/metabolismo
Proteínas Nucleares/metabolismo
Ligação Proteica
Interferência de RNA
RNA Longo não Codificante/metabolismo
Transativadores/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nuclear Proteins); 0 (RNA, Long Noncoding); 0 (Trans-Activators); 0 (Tumor Suppressor Protein p53); 0 (myocardin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02280-y


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[PMID]:28743763
[Au] Autor:Al-Owais MM; Hettiarachchi NT; Kirton HM; Hardy ME; Boyle JP; Scragg JL; Steele DS; Peers C
[Ad] Endereço:Division of Cardiovascular and Diabetes Research, Leeds Institute of Cardiovascular and Metabolic Medicine, Faculty of Medicine and Health, University of Leeds, Leeds, United Kingdom; and.
[Ti] Título:A key role for peroxynitrite-mediated inhibition of cardiac ERG (Kv11.1) K channels in carbon monoxide-induced proarrhythmic early afterdepolarizations.
[So] Source:FASEB J;31(11):4845-4854, 2017 11.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Exposure to CO causes early afterdepolarization arrhythmias. Previous studies in rats have indicated that arrhythmias arose as a result of augmentation of the late Na current. The purpose of the present study was to examine the basis for CO-induced arrhythmias in guinea pig myocytes in which action potentials (APs) more closely resemble those of human myocytes. Whole-cell current- and voltage-clamp recordings were made from isolated guinea pig myocytes as well as from human embryonic kidney 293 (HEK293) cells that express wild-type or a C723S mutant form of ether-a-go-go-related gene (ERG; Kv11.1). We also monitored the formation of peroxynitrite (ONOO ) in HEK293 cells fluorimetrically. CO-applied as the CO-releasing molecule, CORM-2-prolonged the APs and induced early afterdepolarizations in guinea pig myocytes. In HEK293 cells, CO inhibited wild-type, but not C723S mutant, Kv11.1 K currents. Inhibition was prevented by an antioxidant, mitochondrial inhibitors, or inhibition of NO formation. CO also raised ONOO levels, an effect that was reversed by the ONOO scavenger, FeTPPS [5,10,15,20-tetrakis-(4-sulfonatophenyl)-porphyrinato-iron(III)], which also prevented the CO inhibition of Kv11.1 currents and abolished the effects of CO on Kv11.1 tail currents and APs in guinea pig myocytes. Our data suggest that CO induces arrhythmias in guinea pig cardiac myocytes the ONOO -mediated inhibition of Kv11.1 K channels.-Al-Owais, M. M., Hettiarachchi, N. T., Kirton, H. M., Hardy, M. E., Boyle, J. P., Scragg, J. L., Steele, D. S., Peers, C. A key role for peroxynitrite-mediated inhibition of cardiac ERG (Kv11.1) K channels in carbon monoxide-induced proarrhythmic early afterdepolarizations.
[Mh] Termos MeSH primário: Arritmias Cardíacas/metabolismo
Monóxido de Carbono/toxicidade
Canal de Potássio ERG1/metabolismo
Potenciais da Membrana/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Ácido Peroxinitroso/metabolismo
[Mh] Termos MeSH secundário: Animais
Arritmias Cardíacas/induzido quimicamente
Arritmias Cardíacas/genética
Arritmias Cardíacas/patologia
Canal de Potássio ERG1/genética
Cobaias
Células HEK293
Seres Humanos
Metaloporfirinas/farmacologia
Miócitos Cardíacos/patologia
Óxido Nítrico/genética
Óxido Nítrico/metabolismo
Compostos Organometálicos/farmacologia
Ácido Peroxinitroso/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (5,10,15,20-tetrakis(4-sulfonatophenyl)porphyrinato iron(III) chloride); 0 (ERG1 Potassium Channel); 0 (KCNH2 protein, human); 0 (Metalloporphyrins); 0 (Organometallic Compounds); 0 (tricarbonyldichlororuthenium (II) dimer); 14691-52-2 (Peroxynitrous Acid); 31C4KY9ESH (Nitric Oxide); 7U1EE4V452 (Carbon Monoxide)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201700259R


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[PMID]:28610437
[Au] Autor:Song Y; Zhou J; Wang X; Xie X; Zhao Y; Ni F; Huang W; Wang Z; Xiao W
[Ad] Endereço:a Jiangsu Kanion Pharmaceutical Co., Ltd. , Lianyungang , People's Republic of China.
[Ti] Título:A new ferulic acid ester from Rhodiola wallichiana var. cholaensis (Crassulaceae).
[So] Source:Nat Prod Res;32(1):77-84, 2018 Jan.
[Is] ISSN:1478-6427
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A new ferulic acid ester, 6-feruloyloxyhexanoic acid (1), was isolated along with 10 known ones (2-11), from the concentrated water extract of Rhodiola wallichiana var. cholaensis. Their chemical structures were elucidated on the basis of extensive spectroscopic methods including Two-dimensional nuclear magnetic resonance (2D NMR) experiments. Compound 3 was isolated from this plant for the first time. The protective effects against H O -induced myocardial cell injury in cultured H9c2 cells were also evaluated. Compounds 1, 5 and 7-11 provided significant protective effects on H O -induced H9c2 cells injury at the concentration of 25 µg/mL. And the protective effects of compound 1 was also investigated by the oxygen-glucose deprivation/reperfusion (OGD/R) tests.
[Mh] Termos MeSH primário: Caproatos/farmacologia
Cardiotônicos/farmacologia
Ácidos Cumáricos/farmacologia
Rhodiola/química
[Mh] Termos MeSH secundário: Animais
Antioxidantes/química
Antioxidantes/farmacologia
Caproatos/administração & dosagem
Caproatos/química
Cardiotônicos/administração & dosagem
Cardiotônicos/química
Células Cultivadas
Ácidos Cumáricos/administração & dosagem
Ácidos Cumáricos/química
Relação Dose-Resposta a Droga
Ésteres/administração & dosagem
Ésteres/química
Ésteres/farmacologia
Peróxido de Hidrogênio/toxicidade
Espectroscopia de Ressonância Magnética
Estrutura Molecular
Miócitos Cardíacos/citologia
Miócitos Cardíacos/efeitos dos fármacos
Extratos Vegetais/química
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Caproates); 0 (Cardiotonic Agents); 0 (Coumaric Acids); 0 (Esters); 0 (Plant Extracts); BBX060AN9V (Hydrogen Peroxide)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE
[do] DOI:10.1080/14786419.2017.1335724


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[PMID]:28455218
[Au] Autor:Li Y; Asfour H; Bursac N
[Ad] Endereço:Department of Biomedical Engineering, Duke University, United States.
[Ti] Título:Age-dependent functional crosstalk between cardiac fibroblasts and cardiomyocytes in a 3D engineered cardiac tissue.
[So] Source:Acta Biomater;55:120-130, 2017 Jun.
[Is] ISSN:1878-7568
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Complex heterocellular interactions between cardiomyocytes and fibroblasts in the heart involve their bidirectional signaling via cell-cell contacts, paracrine factors, and extracellular matrix (ECM). These interactions vary with heart development and pathology leading to changes in cardiac structure and function. Whether cardiac fibroblasts of different ages interact differentially with cardiomyocytes to distinctly impact their function remains unknown. Here, we explored the direct structural and functional effects of fetal and adult cardiac fibroblasts on cardiomyocytes using a tissue-engineered 3D co-culture system. We show that the age of cardiac fibroblasts is a strong determinant of the structure, function, and molecular properties of co-cultured tissues. In particular, in vitro expanded adult, but not fetal, cardiac fibroblasts significantly deteriorated electrical and mechanical function of the co-cultured cardiomyocytes, as evidenced by slower action potential conduction, prolonged action potential duration, weaker contractions, higher tissue stiffness, and reduced calcium transient amplitude. This functional deficit was associated with structural and molecular signatures of pathological remodeling including fibroblast proliferation, interstitial collagen deposition, and upregulation of pro-fibrotic markers. Our studies imply critical roles of the age of supporting cells in engineering functional cardiac tissues and provide a new physiologically relevant in vitro platform to investigate influence of heterocellular interactions on cardiomyocyte function, development, and disease. STATEMENT OF SIGNIFICANCE: Previous studies have shown that cardiomyocytes and fibroblasts in the heart interact through direct contacts, paracrine factors, and matrix-mediated crosstalk. However, whether cardiac fibroblasts of different ages distinctly impact cardiomyocyte function remains elusive. We employed a tissue-engineered hydrogel-based co-culture system to study interactions of cardiomyocytes with fetal or adult cardiac fibroblasts. We show that the age of cardiac fibroblasts is a strong determinant of the structure, function, and molecular properties of engineered cardiac tissues and that key features of fibrotic myocardium are replicated by supplementing cardiomyocytes with expanded adult but not fetal fibroblasts. These findings relate to implantation of stem cell-derived cardiomyocytes in adult myocardium and warrant further studies of how age and source of non-myocytes impact cardiac function and maturation.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Fibroblastos/metabolismo
Miocárdio/metabolismo
Miócitos Cardíacos/metabolismo
Engenharia Tecidual/métodos
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Fibroblastos/citologia
Miocárdio/citologia
Miócitos Cardíacos/citologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


  8 / 25463 MEDLINE  
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[PMID]:27776917
[Au] Autor:Luconi M; Raimondi L; Di Franco A; Mannucci E
[Ad] Endereço:Endocrinology Unit, Dept. Clinical and Experimental Biomedical Sciences, University of Florence, Viale G. Pieraccini, 6, Florence, Italy.
[Ti] Título:Which is the main molecular target responsible for the cardiovascular benefits in the EMPA-REG OUTCOME trial? A journey through the kidney, the heart and other interesting places.
[So] Source:Nutr Metab Cardiovasc Dis;26(12):1071-1078, 2016 12.
[Is] ISSN:1590-3729
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The results of the EMPA-REG-OUTCOME trial on type 2 diabetic patients at high risk for prior cardiovascular events showed that empagliflozin produces a remarkable reduction in the rates of hospitalization for heart failure (35%), cardiovascular death (38%), and all-cause death (32%). This unexpected cardio-protective action cannot be accounted for by the improvement of "classical" cardiovascular risk factors. AIMS: This review aims at summarizing current knowledge on the cardiovascular action of SGLT2 inhibitors and discuss the different hypotheses formulated to explain the results of the EMPA-REG-OUTCOME-study. DATA SYNTHESIS: We discuss in detail the major cardiovascular outcomes of the study in the light of the potential systemic and myocardial mechanisms of action of the drug. In addition, we propose and speculate on a direct effect of empagliflozin on cardiomyocytes. CONCLUSIONS: The available evidence is insufficient to establish any of the proposed mechanisms of cardiovascular action of empagliflozin. While awaiting for the results of ongoing clinical studies with other SGLT2 inhibitors, the most promising putative mechanisms still deserve to be confirmed with specifically designed, yet unavailable, pre-clinical studies.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/uso terapêutico
Doenças Cardiovasculares/prevenção & controle
Diabetes Mellitus Tipo 2/tratamento farmacológico
Glucosídeos/uso terapêutico
Coração/fisiopatologia
Hipoglicemiantes/uso terapêutico
Rim/efeitos dos fármacos
Miócitos Cardíacos/efeitos dos fármacos
Transportador 2 de Glucose-Sódio/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Compostos Benzidrílicos/efeitos adversos
Doenças Cardiovasculares/mortalidade
Doenças Cardiovasculares/fisiopatologia
Ensaios Clínicos como Assunto
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/mortalidade
Diabetes Mellitus Tipo 2/fisiopatologia
Glucosídeos/efeitos adversos
Seres Humanos
Hipoglicemiantes/efeitos adversos
Rim/metabolismo
Rim/fisiopatologia
Miócitos Cardíacos/metabolismo
Medição de Risco
Fatores de Risco
Transportador 2 de Glucose-Sódio/metabolismo
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Glucosides); 0 (Hypoglycemic Agents); 0 (SLC5A2 protein, human); 0 (Sodium-Glucose Transporter 2); HDC1R2M35U (empagliflozin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:29442001
[Au] Autor:Liu C; Zheng H; Xie L; Zhang J
[Ti] Título:Decreased miR-208 induced ischemia myocardial and reperfusion injury by targeting p21.
[So] Source:Pharmazie;71(12):719-723, 2016 Dec 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Aberrant expression of miR-208 was previously reported in cardiomyocytes after cardiac ischemia reperfusion (CIR) injury. However, the underlying mechanism has never been elucidated. In the current study, the relative level of miR-208 was determined in the hearts of CIR injury mice models using real time PCR. The effect of miR-208 on cardiomyocytes apoptosis was determined by Hoechst staining and annexin V-PI staining. Meanwhile, caspase3 activity was explored using an assay kit. To identify left ventricular fraction and relative wall thickness, the two-dimensional echocardiography was applied. Dual luciferase assay was applied to determine the target gene of miR-208. Compared with normal control, the level of miR-208 was significantly reduced in the hearts of CIR injury mouse models. Further studies revealed that reduction of miR-208 contributed to reactive oxygen species (ROS) production in the cardiomyocytes. We also found that inhibition of miR-208 prompted cardiomyocyte apoptosis. More importantly, the phosphorylation level of Akt and p38 was enhanced in primary cardiomyocytes transfected with miR-208 inhibitor, indicating a potential stress-response after CIR injury in primary cardiomyocytes. Dual luciferase assay and western blot analysis showed that transfection with miR-208 markedly suppressed the protein expression of p21, suggesting p21 was a target gene of miR-208. To conclude, we showed that reduced miR-208 level enhanced cardiomyocyte apoptosis mainly by targeting p21.
[Mh] Termos MeSH primário: MicroRNAs/genética
Isquemia Miocárdica/genética
Traumatismo por Reperfusão Miocárdica/genética
Proteína Oncogênica p21(ras)/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Caspase 3/biossíntese
Caspase 3/genética
Masculino
Camundongos
MicroRNAs/antagonistas & inibidores
Isquemia Miocárdica/fisiopatologia
Traumatismo por Reperfusão Miocárdica/fisiopatologia
Miócitos Cardíacos/metabolismo
Proteína Oncogênica v-akt/metabolismo
Fosforilação
Cultura Primária de Células
Espécies Reativas de Oxigênio/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (Mirn208 microRNA, mouse); 0 (Reactive Oxygen Species); EC 2.7.11.1 (Oncogene Protein v-akt); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 3.4.22.- (Casp3 protein, mouse); EC 3.4.22.- (Caspase 3); EC 3.6.5.2 (Oncogene Protein p21(ras))
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6740


  10 / 25463 MEDLINE  
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[PMID]:29374152
[Au] Autor:Gilsbach R; Schwaderer M; Preissl S; Grüning BA; Kranzhöfer D; Schneider P; Nührenberg TG; Mulero-Navarro S; Weichenhan D; Braun C; Dreßen M; Jacobs AR; Lahm H; Doenst T; Backofen R; Krane M; Gelb BD; Hein L
[Ad] Endereço:Institute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Freiburg, 79104, Freiburg, Germany.
[Ti] Título:Distinct epigenetic programs regulate cardiac myocyte development and disease in the human heart in vivo.
[So] Source:Nat Commun;9(1):391, 2018 01 26.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Epigenetic mechanisms and transcription factor networks essential for differentiation of cardiac myocytes have been uncovered. However, reshaping of the epigenome of these terminally differentiated cells during fetal development, postnatal maturation, and in disease remains unknown. Here, we investigate the dynamics of the cardiac myocyte epigenome during development and in chronic heart failure. We find that prenatal development and postnatal maturation are characterized by a cooperation of active CpG methylation and histone marks at cis-regulatory and genic regions to shape the cardiac myocyte transcriptome. In contrast, pathological gene expression in terminal heart failure is accompanied by changes in active histone marks without major alterations in CpG methylation and repressive chromatin marks. Notably, cis-regulatory regions in cardiac myocytes are significantly enriched for cardiovascular disease-associated variants. This study uncovers distinct layers of epigenetic regulation not only during prenatal development and postnatal maturation but also in diseased human cardiac myocytes.
[Mh] Termos MeSH primário: Epigênese Genética/genética
Miócitos Cardíacos/metabolismo
[Mh] Termos MeSH secundário: Doenças Cardiovasculares/genética
Diferenciação Celular/genética
Diferenciação Celular/fisiologia
Cromatina/genética
Ilhas de CpG/genética
Metilação de DNA/genética
Insuficiência Cardíaca/genética
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chromatin)
[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:180128
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02762-z



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