Base de datos : MEDLINE Búsqueda : corazón [Palabras] Referencias encontradas : 392378 [refinar] Mostrando: 1 .. 10   en el formato [Detallado]

página 1 de 39238

va a la página

1 / 392378

MEDLINE

selecciona para imprimir Fotocopia Texto completo

[PMID]: 23620051 [Au] Autor: Chen Y; Dorn GW [Ad] Dirección: Center for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. [Ti] Título: PINK1-phosphorylated mitofusin 2 is a Parkin receptor for culling damaged mitochondria. [So] Fuente: Science;340(6131):471-5, 2013 Apr 26. [Is] ISSN: 1095-9203 [Cp] País de publicación: United States [La] Idioma: eng [Ab] Resumen: Senescent and damaged mitochondria undergo selective mitophagic elimination through mechanisms requiring two Parkinson's disease factors, the mitochondrial kinase PINK1 (PTEN-induced putative kinase protein 1; PTEN is phosphatase and tensin homolog) and the cytosolic ubiquitin ligase Parkin. The nature of the PINK-Parkin interaction and the identity of key factors directing Parkin to damaged mitochondria are unknown. We show that the mitochondrial outer membrane guanosine triphosphatase mitofusin (Mfn) 2 mediates Parkin recruitment to damaged mitochondria. Parkin bound to Mfn2 in a PINK1-dependent manner; PINK1 phosphorylated Mfn2 and promoted its Parkin-mediated ubiqitination. Ablation of Mfn2 in mouse cardiac myocytes prevented depolarization-induced translocation of Parkin to the mitochondria and suppressed mitophagy. Accumulation of morphologically and functionally abnormal mitochondria induced respiratory dysfunction in Mfn2-deficient mouse embryonic fibroblasts and cardiomyocytes and in Parkin-deficient Drosophila heart tubes, causing dilated cardiomyopathy. Thus, Mfn2 functions as a mitochondrial receptor for Parkin and is required for quality control of cardiac mitochondria. [Mh] Términos MeSH primario: GTP Fosfohidrolasas/metabolismo Mitocondrias Cardíacas/enzimología Miocitos Cardíacos/enzimología Proteínas Quinasas/metabolismo Ubiquitina-Proteína Ligasas/metabolismo [Mh] Términos MeSH secundario: Secuencia de Aminoácidos Animales Autofagia Cardiomiopatías/enzimología Drosophila melanogaster Fibroblastos/ultraestructura GTP Fosfohidrolasas/genética Células HEK293 Humanos Ratones Ratones Mutantes Mitocondrias/enzimología Datos de Secuencia Molecular Miocitos Cardíacos/ultraestructura Fosforilación Ubiquitinación [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL [Nm] Nombre de substancia: EC 2.7.- (Protein Kinases); EC 2.7.11.1 (PTEN-induced putative kinase); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.1.- (Mfn2 protein, mouse); EC 6.3.2.19 (Ubiquitin-Protein Ligases); EC 6.3.2.19 (parkin protein) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130426 [St] Status: MEDLINE [do] DOI: 10.1126/science.1231031

2 / 392378

MEDLINE

selecciona para imprimir Fotocopia Texto completo

[PMID]: 23399703 [Au] Autor: Tzang BS; Hsu TC; Chen TY; Huang CY; Li SL; Kao SH [Ad] Dirección: Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung City, Taiwan. [Ti] Título: Cystamine ameliorates ventricular hypertrophy associated with modulation of IL-6-mediated signaling in lupus-prone mice. [So] Fuente: Life Sci;92(12):719-26, 2013 Apr 9. [Is] ISSN: 1879-0631 [Cp] País de publicación: Netherlands [La] Idioma: eng [Ab] Resumen: AIMS: The aim of this study is to investigate the protective effects of cystamine on lupus-associated cardiac hypertrophy. MAIN METHODS: Balb/c and lupus-prone NZB/W-F1 mice were individually randomized into sham group (saline, n=16) and cystamine group (n=16). Mice received saline or cystamine (100 mmol in 100 µL saline) by daily intraperitoneal injection for 2 consecutive weeks. Morphological, histological, and biochemical alterations were investigated. KEY FINDINGS: Cystamine decreased both left ventricular (LV) mass and LV mass/tissue-to-blood ratio (TBR) in NZB/W-F1 mice (p<0.05), whereas slight effects were observed in Balb/c mice. Moreover, cystamine reduced levels of atrial natriuretic peptide (ANP), C-reactive protein (CRP), heart type-fatty acid binding protein (h-FABP), creatine kinase-MB (CK-MB) and IL-6 in LV tissues of NZB/W-F1 mice (p<0.05). Additionally, in LV tissues of NZB/W-F1 mice, suppression of hypertrophic signaling mediated by IL-6 in response to administration of cystamine was revealed, including phosphorylation of MEK5, ERK5, c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38) (p<0.05). SIGNIFICANCE: Cystamine alleviated LV hypertrophy in NZB/W-F1 mice as a result of decrease in hypertrophic mediators and suppression of IL-6 mediated hypertrophic signaling. [Mh] Términos MeSH primario: Cistamina/uso terapéutico Ventrículos Cardíacos/efectos de drogas Hipertrofia Ventricular Izquierda/complicaciones Hipertrofia Ventricular Izquierda/quimioterapia Interleucina-6/inmunología Lupus Eritematoso Sistémico/complicaciones Sistema de Señalización de Quinasas PAM/efectos de drogas [Mh] Términos MeSH secundario: Animales Antiinflamatorios/farmacología Antiinflamatorios/uso terapéutico Cistamina/farmacología Femenino Proteínas de Unión al GTP/antagonistas & inhibidores Ventrículos Cardíacos/inmunología Ventrículos Cardíacos/patología Hipertrofia Ventricular Izquierda/inmunología Hipertrofia Ventricular Izquierda/patología MAP Quinasa Quinasa 5/inmunología Ratones Ratones Consanguíneos BALB C Ratones Consanguíneos NZB Proteína Quinasa Activada por Mitógeno 7/inmunología Transglutaminasas/antagonistas & inhibidores Proteinas Quinasas Activadas por Mitógeno p38/inmunología [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nombre de substancia: 0 (Anti-Inflammatory Agents); 0 (Interleukin-6); 51-85-4 (Cystamine); EC 2.3.2.- (transglutaminase 2); EC 2.3.2.13 (Transglutaminases); EC 2.7.1.- (MEK5 protein, mouse); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 7); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 2.7.12.2 (MAP Kinase Kinase 5); EC 3.6.1.- (GTP-Binding Proteins) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130319 [St] Status: MEDLINE

3 / 392378

MEDLINE

selecciona para imprimir Fotocopia Texto completo

[PMID]: 23506706 [Au] Autor: Teramoto K; Terasaki F; Isomura T; Ishizaka N [Ti] Título: Assessment of immunoglobulin G4-positive cell infiltration in myopathic heart tissue from patients with severe heart failure. [So] Fuente: Hum Pathol;44(4):676-8, 2013 Apr. [Is] ISSN: 1532-8392 [Cp] País de publicación: United States [La] Idioma: eng [Mh] Términos MeSH primario: Cardiomiopatías/patología Insuficiencia Cardíaca/patología Inmunoglobulina G/metabolismo Miocardio/patología Pericardio/patología Células Plasmáticas/patología [Mh] Términos MeSH secundario: Cardiomiopatías/inmunología Cardiomiopatías/fisiopatología Cardiomiopatías/cirugía Femenino Corazón/fisiopatología Insuficiencia Cardíaca/inmunología Insuficiencia Cardíaca/fisiopatología Insuficiencia Cardíaca/cirugía Pruebas de Función Cardíaca Ventrículos Cardíacos/cirugía Humanos Masculino Mediana Edad Miocardio/inmunología Pericardio/inmunología Células Plasmáticas/inmunología [Pt] Tipo de publicación: LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nombre de substancia: 0 (Immunoglobulin G) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130319 [St] Status: MEDLINE

4 / 392378

MEDLINE

selecciona para imprimir Fotocopia Texto completo

[PMID]: 23438932 [Au] Autor: Du H; Fan J; Ling Z; Woo K; Su L; Chen S; Liu Z; Lan X; Zhou B; Xu Y; Chen W; Xiao P; Yin Y [Ad] Dirección: Department of Cardiology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, China. [Ti] Título: Effect of nifedipine versus telmisartan on prevention of atrial fibrillation recurrence in hypertensive patients. [So] Fuente: Hypertension;61(4):786-92, 2013 Apr. [Is] ISSN: 1524-4563 [Cp] País de publicación: United States [La] Idioma: eng [Ab] Resumen: It is controversial whether angiotensin II receptor blockers provide better protection than calcium antagonists against atrial fibrillation (AF) recurrence in hypertensive patients. This study was designed to compare the effect of nifedipine- and telmisartan-based antihypertensive treatments for preventing AF recurrence in hypertensive patients with paroxysmal AF. A total of 149 hypertensive patients with paroxysmal AF were randomized to nifedipine- or telmisartan-based antihypertensive treatment groups. The target blood pressure (BP) was <130/80 mm Hg. Clinic BP, ECG, Holter monitoring, and echocardiography were followed up for 2 years. The primary end point was the incidence of overall and persistent AF recurrence. During follow-up, there was no statistical difference in the rate of patients lowering to target BP between both groups, whereas nifedipine group had slightly better BP control but similar heart rate control at 24 months. The incidence of AF recurrence was similar in both groups (nifedipine versus telmisartan: 58.7% versus 55.4%; P=0.742), and Kaplan-Meier analysis showed no significant difference in the freedom from AF recurrence (log-rank test; P=0.48). However, the rate of developing persistent AF in telmisartan group was lower than that in nifedipine group (5.4% versus 16.0%; P=0.035). Patients in telmisartan group had lower values of left atrial diameter, left atrial volume index, and left ventricular mass index at the end of follow-up. The effects of telmisartan in preventing AF recurrences in hypertensive patients with paroxysmal AF after intensive lowering BP is similar to that of nifedipine, but telmisartan has more potent effects on preventing progression to persistent AF. [Mh] Términos MeSH primario: Fibrilación Atrial/quimioterapia Bencimidazoles/administración & dosificación Benzoatos/administración & dosificación Presión Sanguínea/efectos de drogas Frecuencia Cardíaca/efectos de drogas Hipertensión/complicaciones Nifedipino/administración & dosificación [Mh] Términos MeSH secundario: Bloqueadores del Receptor Tipo 1 de Angiotensina II/administración & dosificación Fibrilación Atrial/etiología Fibrilación Atrial/fisiopatología Presión Sanguínea/fisiología Bloqueadores de los Canales de Calcio/administración & dosificación Relación Dosis-Respuesta a Droga Ecocardiografía Electrocardiografía Femenino Estudios de Seguimiento Atrios Cardíacos/efectos de drogas Atrios Cardíacos/ultrasonografía Humanos Hipertensión/quimioterapia Hipertensión/fisiopatología Masculino Mediana Edad Estudios Prospectivos Recurrencia/prevención & control Resultado del Tratamiento [Pt] Tipo de publicación: COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nombre de substancia: 0 (Angiotensin II Type 1 Receptor Blockers); 0 (Benzimidazoles); 0 (Benzoates); 0 (Calcium Channel Blockers); 144701-48-4 (telmisartan); 21829-25-4 (Nifedipine) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130314 [St] Status: MEDLINE [do] DOI: 10.1161/HYPERTENSIONAHA.111.202309

5 / 392378

MEDLINE

selecciona para imprimir Fotocopia Texto completo

[PMID]: 23424238 [Au] Autor: Mewton N; Opdahl A; Choi EY; Almeida AL; Kawel N; Wu CO; Burke GL; Liu S; Liu K; Bluemke DA; Lima JA [Ad] Dirección: Department of Medicine, Division of Cardiology, School of Medicine, Johns Hopkins University, Baltimore, MD 21287, USA. [Ti] Título: Left ventricular global function index by magnetic resonance imaging--a novel marker for assessment of cardiac performance for the prediction of cardiovascular events: the multi-ethnic study of atherosclerosis. [So] Fuente: Hypertension;61(4):770-8, 2013 Apr. [Is] ISSN: 1524-4563 [Cp] País de publicación: United States [La] Idioma: eng [Ab] Resumen: Left ventricular (LV) function is generally assessed independent of structural remodeling and vice versa. The purpose of this study was to evaluate a novel LV global function index (LVGFI) that integrates LV structure with global function and to assess its predictive value for cardiovascular (CV) events throughout adult life in a multiethnic population of men and women without history of CV diseases at baseline. A total of 5004 participants in the Multi-Ethnic Study of Atherosclerosis underwent a cardiac magnetic resonance study and were followed up for a median of 7.2 years. The LVGFI by cardiac magnetic resonance was defined by the ratio of stroke volume divided by LV total volume defined as the sum of mean LV cavity and myocardial volumes. Cox proportional hazard models were constructed to predict the end points of heart failure, hard CV events, and a combined end point of all CV events after adjustment for established risk factors, calcium score, and biomarkers. A total of 579 (11.6%) CV events were observed during the follow-up period. In adjusted models, the end points of heart failure, hard CV events, and all events were all significantly associated with LVGFI (heart failure, hazard ratio=0.64, P<0.0001; hard CV events, hazard ratio=0.79, P=0.007; all events, hazard ratio=0.79, P<0.0001). LVGFI had a significant independent predictive value in the multivariable models for all CV event categories. The LVGFI was a powerful predictor of incident HF, hard CV events, and a composite end point, including all events in this multiethnic cohort. [Mh] Términos MeSH primario: Aterosclerosis/fisiopatología Grupos Étnicos Ventrículos Cardíacos/fisiopatología Imagen por Resonancia Cinemagnética/métodos Función Ventricular Izquierda/fisiología [Mh] Términos MeSH secundario: Anciano Aterosclerosis/diagnóstico Aterosclerosis/etnología Femenino Estudios de Seguimiento Ventrículos Cardíacos/patología Humanos Masculino Mediana Edad Prevalencia Modelos de Riesgos Proporcionales Estudios Prospectivos Valores de Referencia Factores de Riesgo Volumen Sistólico Estados Unidos/epidemiología [Pt] Tipo de publicación: COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130314 [St] Status: MEDLINE [do] DOI: 10.1161/HYPERTENSIONAHA.111.198028

6 / 392378

MEDLINE

selecciona para imprimir Fotocopia Texto completo

[PMID]: 23424234 [Au] Autor: McComb C; Berry C [Ti] Título: Prognostic importance of a new measure of global systolic heart function in healthy adults. [So] Fuente: Hypertension;61(4):762-4, 2013 Apr. [Is] ISSN: 1524-4563 [Cp] País de publicación: United States [La] Idioma: eng [Mh] Términos MeSH primario: Aterosclerosis/fisiopatología Grupos Étnicos Ventrículos Cardíacos/fisiopatología Imagen por Resonancia Cinemagnética/métodos Función Ventricular Izquierda/fisiología [Mh] Términos MeSH secundario: Femenino Humanos Masculino [Pt] Tipo de publicación: COMMENT; EDITORIAL; RESEARCH SUPPORT, NON-U.S. GOV'T [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130314 [St] Status: MEDLINE [do] DOI: 10.1161/HYPERTENSIONAHA.112.199992

7 / 392378

MEDLINE

selecciona para imprimir Fotocopia Texto completo

[PMID]: 23381794 [Au] Autor: Dai Y; Khaidakov M; Wang X; Ding Z; Su W; Price E; Palade P; Chen M; Mehta JL [Ad] Dirección: Cardiovascular Division, UA Little Rock, AR 72212, USA. mehtajl@uams.edu [Ti] Título: MicroRNAs involved in the regulation of postischemic cardiac fibrosis. [So] Fuente: Hypertension;61(4):751-6, 2013 Apr. [Is] ISSN: 1524-4563 [Cp] País de publicación: United States [La] Idioma: eng [Mh] Términos MeSH primario: MicroARNs/fisiología Infarto del Miocardio/complicaciones Miocardio/patología [Mh] Términos MeSH secundario: Fibrosis/etiología Fibrosis/genética Fibrosis/patología Humanos Infarto del Miocardio/genética Infarto del Miocardio/patología [Pt] Tipo de publicación: JOURNAL ARTICLE; REVIEW [Nm] Nombre de substancia: 0 (MicroRNAs) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130314 [St] Status: MEDLINE [do] DOI: 10.1161/HYPERTENSIONAHA.111.00654

8 / 392378

MEDLINE

selecciona para imprimir Fotocopia Texto completo

[PMID]: 23295156 [Au] Autor: Zambrano S; Blanca AJ; Ruiz-Armenta MV; Miguel-Carrasco JL; Arévalo M; Vázquez MJ; Mate A; Vázquez CM [Ad] Dirección: Departamento de Fisiología, Facultad de Farmacia, Universidad de Sevilla, c/Profesor García González 2, 41012 Sevilla, Spain. [Ti] Título: L-Carnitine protects against arterial hypertension-related cardiac fibrosis through modulation of PPAR-γ expression. [So] Fuente: Biochem Pharmacol;85(7):937-44, 2013 Apr 1. [Is] ISSN: 1873-2968 [Cp] País de publicación: England [La] Idioma: eng [Ab] Resumen: Cardiac fibrosis is a pathogenic factor in a variety of cardiovascular diseases and is characterized by an abnormal accumulation of extracellular matrix protein that leads to cardiac dysfunction. l-Carnitine (LC) plays an essential role in the ß-oxidation of long-chain fatty acids in lipid metabolism. We have previously demonstrated the beneficial effects of LC in hypertensive rats. The aim of this study was to analyze the effect of LC on arterial hypertension-associated cardiac fibrosis and to explore the mechanisms of LC action. To this end, four groups of rats were used: Wistar (control), rats treated with 400mg/kg/day of LC, rats treated with 25mg/kg/day of l-NAME (to induce hypertension), and rats treated with LC+l-NAME simultaneously. We found an elevation in the myocardial expression of profibrotic factors (TGF-ß1 and CTGF), types I and III of collagen, and NADPH oxidase subunits (NOX2 and NOX4), in hypertensive rats when compared with normotensive ones. In addition, an increase in myocardial fibrosis was also found in the l-NAME group. These results were accompanied by a down-regulation of PPAR-γ in the heart of hypertensive animals. When hypertensive rats were treated with LC, all these alterations were reversed. Moreover, a significant negative correlation was observed between myocardial interstitial fibrosis and mRNA expression of PPAR-γ. In conclusion, the reduction of cardiac fibrosis and the down-regulation of NOX2, NOX4, TGF-ß1 and CTGF induced by LC might be, at least in part, mediated by an upregulation of PPAR-γ, which leads to a reduction on hypertension-related cardiac fibrosis. [Mh] Términos MeSH primario: Antihipertensivos/farmacología Carnitina/farmacología Hipertensión/quimioterapia Miocardio/patología PPAR gamma/metabolismo [Mh] Términos MeSH secundario: Animales Antihipertensivos/uso terapéutico Carnitina/química Carnitina/uso terapéutico Colágeno Tipo I/metabolismo Colágeno Tipo II/metabolismo Factor de Crecimiento del Tejido Conjuntivo/metabolismo Fibrosis Hipertensión/inducido químicamente Hipertensión/patología Masculino Glicoproteínas de Membrana/metabolismo Miocardio/metabolismo NADPH Oxidasa/metabolismo NG-Nitroarginina Metil Éster Ratas Ratas Wistar Factor de Crecimiento Transformador beta1/metabolismo [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nombre de substancia: 0 (Antihypertensive Agents); 0 (Collagen Type I); 0 (Collagen Type II); 0 (Membrane Glycoproteins); 0 (PPAR gamma); 0 (Transforming Growth Factor beta1); 139568-91-5 (Connective Tissue Growth Factor); 50903-99-6 (NG-Nitroarginine Methyl Ester); 541-15-1 (Carnitine); EC 1.6.- (Cybb protein, rat); EC 1.6.- (Nox4 protein, rat); EC 1.6.3.1 (NADPH Oxidase) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130307 [St] Status: MEDLINE

9 / 392378

MEDLINE

selecciona para imprimir Fotocopia Texto completo

[PMID]: 23275620 [Au] Autor: Chen J; Petrov A; Yaniz-Galende E; Liang L; de Haas HJ; Narula J; Hajjar RJ [Ad] Dirección: Cardiovascular Research Center, Mount Sinai School of Medicine, New York, NY 10029, USA. [Ti] Título: The impact of pressure overload on coronary vascular changes following myocardial infarction in rats. [So] Fuente: Am J Physiol Heart Circ Physiol;304(5):H719-28, 2013 Mar 1. [Is] ISSN: 1522-1539 [Cp] País de publicación: United States [La] Idioma: eng [Ab] Resumen: This study investigates the impact of pressure overload on vascular changes after myocardial infarction (MI) in rats. To evaluate the effect of pressure overload, MI was induced in three groups: 1) left coronary artery ligation for 1 mo (MI-1m), 2) ischemia 30 min/reperfusion for 1 mo (I/R-1m), and 3) ischemia-reperfusion (I/R) was performed after pressure overload induced by aortic banding for 2 mo; 1 mo post-I/R, aortic constriction was released (Ab+I/R+DeAb). Heart function was assessed by echocardiography and in vivo hemodynamics. Resin casting and three-dimensional imaging with microcomputed tomography were used to characterize changes in coronary vasculature. TTC (triphenyltetrazohum chloride) staining and Masson's Trichrome were conducted in parallel experiments. In normal rats, MI induced by I/R and permanent occlusion was transmural or subendocardial. Occluded arterial branches vanished in MI-1m rats. A short residual tail was retained, distal to the occluded site in the ischemic area in I/R-1m hearts. Vascular pathological changes in transmural MI mostly occurred in ischemic areas and remote vasculature remained normal. In pressure overloaded rats, I/R injury induced a sub-MI in which ischemia was transmural, but myocardium in the involved area had survived. The ischemic arterial branches were preserved even though the capillaries were significantly diminished and the pathological changes were extended to remote areas, characterized by fibrosis, atrial thrombus, and pulmonary edema in the Ab+I/R+DeAb group. Pressure overload could increase vascular tolerance to I/R injury, but also trigger severe global ventricular fibrosis and results in atrial thrombus and pulmonary edema. [Mh] Términos MeSH primario: Circulación Coronaria/fisiología Vasos Coronarios/fisiología Insuficiencia Cardíaca/fisiopatología Infarto del Miocardio/fisiopatología Presión Ventricular/fisiología [Mh] Términos MeSH secundario: Animales Capilares/fisiología Capilares/radiografía Capilares/ultrasonografía Técnicas de Imagen Cardíaca Vasos Coronarios/radiografía Vasos Coronarios/ultrasonografía Modelos Animales de Enfermedad Ecocardiografía Fibrosis/diagnóstico Fibrosis/fisiopatología Insuficiencia Cardíaca/diagnóstico Masculino Infarto del Miocardio/diagnóstico Daño por Reperfusión Miocárdica/diagnóstico Daño por Reperfusión Miocárdica/fisiopatología Miocardio/patología Ratas Ratas Sprague-Dawley Tomografía Computarizada por Rayos X [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, P.H.S. [Em] Mes de ingreso: 1304 [Cu] Fecha actualización por clase: 130506 [Lr] Fecha última revisión: 130506 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130304 [St] Status: MEDLINE [do] DOI: 10.1152/ajpheart.00793.2012

10 / 392378

MEDLINE

selecciona para imprimir Fotocopia PubMed Central Texto completo Texto completo

[PMID]: 23307558 [Au] Autor: Li S; Guo W; Dewey CN; Greaser ML [Ad] Dirección: Muscle Biology Laboratory, Department of Animal Sciences, University of Wisconsin-Madison, Madison, WI 53706, USA. [Ti] Título: Rbm20 regulates titin alternative splicing as a splicing repressor. [So] Fuente: Nucleic Acids Res;41(4):2659-72, 2013 Feb 1. [Is] ISSN: 1362-4962 [Cp] País de publicación: England [La] Idioma: eng [Ab] Resumen: Titin, a sarcomeric protein expressed primarily in striated muscles, is responsible for maintaining the structure and biomechanical properties of muscle cells. Cardiac titin undergoes developmental size reduction from 3.7 megadaltons in neonates to primarily 2.97 megadaltons in the adult. This size reduction results from gradually increased exon skipping between exons 50 and 219 of titin mRNA. Our previous study reported that Rbm20 is the splicing factor responsible for this process. In this work, we investigated its molecular mechanism. We demonstrate that Rbm20 mediates exon skipping by binding to titin pre-mRNA to repress the splicing of some regions; the exons/introns in these Rbm20-repressed regions are ultimately skipped. Rbm20 was also found to mediate intron retention and exon shuffling. The two Rbm20 speckles found in nuclei from muscle tissues were identified as aggregates of Rbm20 protein on the partially processed titin pre-mRNAs. Cooperative repression and alternative 3' splice site selection were found to be used by Rbm20 to skip different subsets of titin exons, and the splicing pathway selected depended on the ratio of Rbm20 to other splicing factors that vary with tissue type and developmental age. [Mh] Términos MeSH primario: Empalme Alternativo Proteínas Musculares/genética Proteínas Quinasas/genética Proteínas de Unión al ARN/metabolismo [Mh] Términos MeSH secundario: Animales Línea Celular Núcleo Celular/química Exonas Corazón/crecimiento & desarrollo Proteínas Musculares/metabolismo Miocitos Cardíacos/metabolismo Isoformas de Proteínas/genética Isoformas de Proteínas/metabolismo Proteínas Quinasas/metabolismo Sitios de Empalme de ARN Proteínas de Unión al ARN/análisis Ratas [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S. [Nm] Nombre de substancia: 0 (Muscle Proteins); 0 (Protein Isoforms); 0 (RBM20 protein, rat); 0 (RNA Splice Sites); 0 (RNA-Binding Proteins); 0 (connectin); 0 (ribonucleic acid binding motif protein 20, human); EC 2.7.- (Protein Kinases) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130220 [St] Status: MEDLINE [do] DOI: 10.1093/nar/gks1362

---

página 1 de 39238

va a la página

Refinar la búsqueda

Base de datos : MEDLINE

Formulario avanzado

		Buscar	en el campo
1			PalabrasDescriptor de asuntoDescriptor de asunto primarioLímitesAutorPalabras del títuloPalabras del resumenIdiomaPaís de publicaciónNombre de substanciaNombre personal como asuntoRevistaAsunto de RevistaISSNTipo de publicaciónIdentificador únicoMes de ingresoAño de publicaciónTexto completoActualización por claseCategoria DeCSCategoria DeCS explodidaCategoria CIE-10SubSetsPaís de AfiliaciónAfiliación
2	and or and not		PalabrasDescriptor de asuntoDescriptor de asunto primarioLímitesAutorPalabras del títuloPalabras del resumenIdiomaPaís de publicaciónNombre de substanciaNombre personal como asuntoRevistaAsunto de RevistaISSNTipo de publicaciónIdentificador únicoMes de ingresoAño de publicaciónTexto completoActualización por claseCategoria DeCSCategoria DeCS explodidaCategoria CIE-10SubSetsPaís de AfiliaciónAfiliación
3	and or and not		PalabrasDescriptor de asuntoDescriptor de asunto primarioLímitesAutorPalabras del títuloPalabras del resumenIdiomaPaís de publicaciónNombre de substanciaNombre personal como asuntoRevistaAsunto de RevistaISSNTipo de publicaciónIdentificador únicoMes de ingresoAño de publicaciónTexto completoActualización por claseCategoria DeCSCategoria DeCS explodidaCategoria CIE-10SubSetsPaís de AfiliaciónAfiliación

Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPS/OMS - Centro Latinoamericano y del Caribe de Información en Ciencias de la Salud