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  1 / 26053 MEDLINE  
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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] Dirección: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] Fuente:Nat Commun;9(1):428, 2018 01 30.
[Is] ISSN:2041-1723
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen: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] Términos MeSH primario: Ventrículos Cardíacos/citología
Miocardio/citología
Miocitos Cardíacos/citología
Regeneración/genética
Proteínas de Dominio T Box/genética
Pez Cebra/genética
[Mh] Términos MeSH secundario: Animales
Animales Modificados Genéticamente
Diferenciación Celular
Linaje de la Célula/genética
Rastreo Celular
Embrión no Mamífero
Regulación del Desarrollo de la Expresión Génica
Genes Reporteros
Proteínas Fluorescentes Verdes/genética
Proteínas Fluorescentes Verdes/metabolismo
Ventrículos Cardíacos/crecimiento & desarrollo
Ventrículos Cardíacos/metabolismo
Proteínas Luminiscentes/genética
Proteínas Luminiscentes/metabolismo
Miocardio/metabolismo
Miocitos Cardíacos/metabolismo
Cadenas Ligeras de Miosina/genética
Cadenas Ligeras de Miosina/metabolismo
Organogénesis/genética
Células Madre/citología
Células Madre/metabolismo
Proteínas de Dominio T Box/deficiencia
Pez Cebra/crecimiento & desarrollo
Pez Cebra/metabolismo
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
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] Mes de ingreso:1803
[Cu] Fecha actualización por clase:180307
[Lr] Fecha última revisión:180307
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento: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] Dirección: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] Fuente:Cardiovasc Res;113(6):598-608, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen: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] Términos MeSH primario: Cardiomegalia/patología
Cardiomiopatías/tratamiento farmacológico
Fármacos Cardiovasculares/farmacología
Insuficiencia Cardíaca/prevención & control
Miocitos Cardíacos/efectos de los fármacos
Periodo Posparto/sangre
Relaxina/farmacología
[Mh] Términos MeSH secundario: Adulto
Animales
Biomarcadores/sangre
Cardiomegalia/sangre
Cardiomegalia/fisiopatología
Cardiomiopatías/sangre
Cardiomiopatías/patología
Cardiomiopatías/fisiopatología
Estudios de Casos y Controles
Modelos Animales de Enfermedad
Femenino
Insuficiencia Cardíaca/sangre
Insuficiencia Cardíaca/patología
Insuficiencia Cardíaca/fisiopatología
Seres Humanos
Ratones Noqueados
Miocitos Cardíacos/metabolismo
Miocitos Cardíacos/patología
Embarazo
Prolactina/sangre
Ratas
Proteínas Recombinantes/farmacología
Sistema de Registros
Relaxina/sangre
Factor de Transcripción STAT3/deficiencia
Factor de Transcripción STAT3/genética
Factor de Transcripción STAT5/metabolismo
Transducción de Señales/efectos de los fármacos
Volumen Sistólico
Función Ventricular Izquierda
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Nm] Nombre de substancia:
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] Mes de ingreso:1802
[Cu] Fecha actualización por clase:180308
[Lr] Fecha última revisión:180308
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento: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] Dirección: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] Fuente:Zhonghua Shao Shang Za Zhi;34(1):21-28, 2018 Jan 20.
[Is] ISSN:1009-2587
[Cp] País de publicación:China
[La] Idioma:chi
[Ab] Resumen: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] Términos MeSH primario: Quemaduras
MicroARNs/genética
Miocardio/metabolismo
Sirtuina 1/metabolismo
[Mh] Términos MeSH secundario: Animales
Western Blotting
Caspasa 3/genética
Caspasa 3/metabolismo
Interleucina-1beta
Miocardio/patología
Miocitos Cardíacos
ARN Mensajero/genética
Ratas
Ratas Sprague-Dawley
Reacción en Cadena en Tiempo Real de la Polimerasa
Sirtuina 1/genética
Estilbenos
Factor de Necrosis Tumoral alfa/genética
Factor de Necrosis Tumoral alfa/metabolismo
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Nm] Nombre de substancia:
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] Mes de ingreso:1803
[Cu] Fecha actualización por clase:180306
[Lr] Fecha última revisión:180306
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:180129
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1009-2587.2018.01.005


  4 / 26053 MEDLINE  
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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] Dirección: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] Fuente:Nat Commun;9(1):29, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen: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] Términos MeSH primario: Autofagia/genética
Infarto del Miocardio/genética
Proteínas Nucleares/genética
ARN Largo no Codificante/genética
Transactivadores/genética
Activación Transcripcional
Proteína p53 Supresora de Tumor/genética
[Mh] Términos MeSH secundario: Animales
Animales Recién Nacidos
Células Cultivadas
Ratones
Infarto del Miocardio/patología
Daño por Reperfusión Miocárdica/genética
Daño por Reperfusión Miocárdica/metabolismo
Miocitos Cardíacos/metabolismo
Proteínas Nucleares/metabolismo
Unión Proteica
Interferencia de ARN
ARN Largo no Codificante/metabolismo
Transactivadores/metabolismo
Proteína p53 Supresora de Tumor/metabolismo
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Nuclear Proteins); 0 (RNA, Long Noncoding); 0 (Trans-Activators); 0 (Tumor Suppressor Protein p53); 0 (myocardin)
[Em] Mes de ingreso:1803
[Cu] Fecha actualización por clase:180306
[Lr] Fecha última revisión:180306
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento: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] Dirección: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] Fuente:FASEB J;31(11):4845-4854, 2017 11.
[Is] ISSN:1530-6860
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen: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] Términos MeSH primario: Arritmias Cardíacas/metabolismo
Monóxido de Carbono/toxicidad
Canal de Potasio ERG1/metabolismo
Potenciales de la Membrana/efectos de los fármacos
Miocitos Cardíacos/metabolismo
Ácido Peroxinitroso/metabolismo
[Mh] Términos MeSH secundario: Animales
Arritmias Cardíacas/inducido químicamente
Arritmias Cardíacas/genética
Arritmias Cardíacas/patología
Canal de Potasio ERG1/genética
Cobayas
Células HEK293
Seres Humanos
Metaloporfirinas/farmacología
Miocitos Cardíacos/patología
Óxido Nítrico/genética
Óxido Nítrico/metabolismo
Compuestos Organometálicos/farmacología
Ácido Peroxinitroso/genética
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
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] Mes de ingreso:1711
[Cu] Fecha actualización por clase:180306
[Lr] Fecha última revisión:180306
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170727
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201700259R


  6 / 26053 MEDLINE  
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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] Dirección: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] Fuente:Nat Prod Res;32(1):77-84, 2018 Jan.
[Is] ISSN:1478-6427
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen: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] Términos MeSH primario: Caproatos/farmacología
Cardiotónicos/farmacología
Ácidos Cumáricos/farmacología
Rhodiola/química
[Mh] Términos MeSH secundario: Animales
Antioxidantes/química
Antioxidantes/farmacología
Caproatos/administración & dosificación
Caproatos/química
Cardiotónicos/administración & dosificación
Cardiotónicos/química
Células Cultivadas
Ácidos Cumáricos/administración & dosificación
Ácidos Cumáricos/química
Relación Dosis-Respuesta a Droga
Ésteres/administración & dosificación
Ésteres/química
Ésteres/farmacología
Peróxido de Hidrógeno/toxicidad
Espectroscopía de Resonancia Magnética
Estructura Molecular
Miocitos Cardíacos/citología
Miocitos Cardíacos/efectos de los fármacos
Extractos Vegetales/química
Ratas
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Nm] Nombre de substancia:
0 (Antioxidants); 0 (Caproates); 0 (Cardiotonic Agents); 0 (Coumaric Acids); 0 (Esters); 0 (Plant Extracts); BBX060AN9V (Hydrogen Peroxide)
[Em] Mes de ingreso:1803
[Cu] Fecha actualización por clase:180301
[Lr] Fecha última revisión:180301
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170615
[St] Status:MEDLINE
[do] DOI:10.1080/14786419.2017.1335724


  7 / 26053 MEDLINE  
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[PMID]:28455218
[Au] Autor:Li Y; Asfour H; Bursac N
[Ad] Dirección: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] Fuente:Acta Biomater;55:120-130, 2017 Jun.
[Is] ISSN:1878-7568
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen: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] Términos MeSH primario: Envejecimiento/metabolismo
Fibroblastos/metabolismo
Miocardio/metabolismo
Miocitos Cardíacos/metabolismo
Ingeniería de Tejidos/métodos
[Mh] Términos MeSH secundario: Animales
Células Cultivadas
Fibroblastos/citología
Miocardio/citología
Miocitos Cardíacos/citología
Ratas
Ratas Sprague-Dawley
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1803
[Cu] Fecha actualización por clase:180301
[Lr] Fecha última revisión:180301
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170430
[St] Status:MEDLINE


  8 / 26053 MEDLINE  
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[PMID]:27776917
[Au] Autor:Luconi M; Raimondi L; Di Franco A; Mannucci E
[Ad] Dirección: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] Fuente:Nutr Metab Cardiovasc Dis;26(12):1071-1078, 2016 12.
[Is] ISSN:1590-3729
[Cp] País de publicación:Netherlands
[La] Idioma:eng
[Ab] Resumen: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] Términos MeSH primario: Compuestos de Bencidrilo/uso terapéutico
Enfermedades Cardiovasculares/prevención & control
Diabetes Mellitus Tipo 2/tratamiento farmacológico
Glucósidos/uso terapéutico
Corazón/fisiopatología
Hipoglucemiantes/uso terapéutico
Riñón/efectos de los fármacos
Miocitos Cardíacos/efectos de los fármacos
Transportador 2 de Sodio-Glucosa/antagonistas & inhibidores
[Mh] Términos MeSH secundario: Animales
Compuestos de Bencidrilo/efectos adversos
Enfermedades Cardiovasculares/mortalidad
Enfermedades Cardiovasculares/fisiopatología
Ensayos Clínicos como Asunto
Diabetes Mellitus Tipo 2/sangre
Diabetes Mellitus Tipo 2/mortalidad
Diabetes Mellitus Tipo 2/fisiopatología
Glucósidos/efectos adversos
Seres Humanos
Hipoglucemiantes/efectos adversos
Riñón/metabolismo
Riñón/fisiopatología
Miocitos Cardíacos/metabolismo
Medición de Riesgo
Factores de Riesgo
Transportador 2 de Sodio-Glucosa/metabolismo
Factores de Tiempo
Resultado del Tratamiento
[Pt] Tipo de publicación:JOURNAL ARTICLE; REVIEW
[Nm] Nombre de substancia:
0 (Benzhydryl Compounds); 0 (Glucosides); 0 (Hypoglycemic Agents); 0 (SLC5A2 protein, human); 0 (Sodium-Glucose Transporter 2); HDC1R2M35U (empagliflozin)
[Em] Mes de ingreso:1707
[Cu] Fecha actualización por clase:180302
[Lr] Fecha última revisión:180302
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:161026
[St] Status:MEDLINE


  9 / 26053 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] Fuente:Pharmazie;71(12):719-723, 2016 Dec 01.
[Is] ISSN:0031-7144
[Cp] País de publicación:Germany
[La] Idioma:eng
[Ab] Resumen: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] Términos MeSH primario: MicroARNs/genética
Isquemia Miocárdica/genética
Daño por Reperfusión Miocárdica/genética
Proteína Oncogénica p21(ras)/genética
[Mh] Términos MeSH secundario: Animales
Apoptosis/efectos de los fármacos
Caspasa 3/biosíntesis
Caspasa 3/genética
Masculino
Ratones
MicroARNs/antagonistas & inhibidores
Isquemia Miocárdica/fisiopatología
Daño por Reperfusión Miocárdica/fisiopatología
Miocitos Cardíacos/metabolismo
Proteína Oncogénica v-akt/metabolismo
Fosforilación
Cultivo Primario de Células
Especies Reactivas de Oxígeno/metabolismo
Proteínas Quinasas p38 Activadas por Mitógenos/metabolismo
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Nm] Nombre de substancia:
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] Mes de ingreso:1802
[Cu] Fecha actualización por clase:180227
[Lr] Fecha última revisión:180227
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6740


  10 / 26053 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] Dirección: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] Fuente:Nat Commun;9(1):391, 2018 01 26.
[Is] ISSN:2041-1723
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen: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] Términos MeSH primario: Epigénesis Genética/genética
Miocitos Cardíacos/metabolismo
[Mh] Términos MeSH secundario: Enfermedades Cardiovasculares/genética
Diferenciación Celular/genética
Diferenciación Celular/fisiología
Cromatina/genética
Islas de CpG/genética
Metilación de ADN/genética
Insuficiencia Cardíaca/genética
Seres Humanos
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Chromatin)
[Em] Mes de ingreso:1802
[Cu] Fecha actualización por clase:180226
[Lr] Fecha última revisión:180226
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:180128
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02762-z



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