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Id: lil-750119
Autor: Abath Neto, Osório Lopes.
Título: Estudo clínico, histológico e molecular da miopatia centronuclear / A clinical, histological and molecular study of centronuclear myopathy.
Fonte: São Paulo; s.n; 2014. [208] p. ilus, tab.
Idioma: pt.
Tese: Apresentada a Universidade de São Paulo. Faculdade de Medicina para obtenção do grau de Doutor.
Resumo: Introdução: A miopatia centronuclear é uma doença muscular congênita com apresentação clínica heterogênea, caracterizada histologicamente pela proeminência de fibras musculares com núcleos centralizados. Três formas são reconhecidas: neonatal grave, com herança ligada ao X e envolvimento do gene MTM1; autossômica dominante, com início geralmente tardio e curso mais leve, associada a mutações no gene DNM2; e autossômica recessiva, com gravidade intermediária entre as outras formas e envolvimento dos genes BIN1, RYR1 ou TTN. Apesar da identificação dos principais genes responsáveis pela doença, os métodos usuais de diagnóstico genético não encontram mutações em cerca da metade dos casos. Objetivo: O objetivo deste estudo foi a caracterização clínica, histológica e molecular de pacientes brasileiros portadores de miopatia centronuclear. Métodos: Laudos de dois bancos de biópsia muscular foram usados para identificar pacientes com diagnóstico de miopatia centronuclear nos últimos dez anos. As lâminas das biópsias foram revisadas e analisadas, e as famílias correspondentes convocadas para aplicação de protocolo clínico e coleta de sangue periférico para extração de DNA genômico. As famílias foram estudadas para os genes conhecidos por sequenciamento Sanger, MLPA, painel de genes implicados em doenças neuromusculares ou sequenciamento de exoma. Resultados: Foram convocados 24 pacientes provenientes de 21 famílias, em 16 das quais foi possível estabelecer o diagnóstico molecular. As 7 famílias com a forma neonatal grave constituíam um grupo homogêneo clínica e histologicamente, e mutações novas e conhecidas foram encontradas no gene MTM1 em 6 destas. Dois meninos deste grupo, com evolução estável, tiveram óbito súbito por choque hipovolêmico subsequente a rompimento de cisto hepático. O gene MTM1 também foi implicado em uma menina portadora manifestante, com quadro mais leve, na forma de uma macrodeleção em heterozigose, detectada por MPLA...

Introduction: Centronuclear myopathy is a heterogeneous congenital muscle disease, characterized by the prominence of centralized nuclei in muscle fibers. Three disease forms are recognized: a severe neonatal, X-linked form caused by mutations in the MTM1 gene; an autosomal dominant, late-onset milder form, associated to the DNM2 gene; and an autosomal recessive form, with intermediate severity, so far with the BIN1, RYR1 or TTN genes implicated. In spite of the identification of these genes, usual molecular diagnostic methods don't yield a molecular diagnosis in about half of cases. Objetives: The aim of this work was to study clinical, histological, and molecular aspects of centronuclear myopathy Brazilian patients. Methods: Reports taken from two muscle biopsy banks were used to identify centronuclear myopathy patients in the last ten years. Biopsy slides were reviewed and analyzed, and corresponding families recruited to apply a clinical protocol and to draw peripheral blood to extract genomic DNA. Families were studied for known genes via Sanger sequencing, MLPA, panel of genes implicated in neuromuscular diseases, or exome sequencing. Results: Twentyfour patients out of 21 families were recruited, and in 16 families molecular diagnosis was established. The 7 families with the severe neonatal form amounted to a clinically and histologically homogeneous group, and mutations, both known and novel, were found in the MTM1 gene in 6 of these. Two boys of this group, with a stable course, died suddenly of hypovolemic shock due to a hepatic cyst rupture. The MTM1 gene was also implicated in the case of a mild manifesting carrier girl with a heterozygous macrodeletion detected via MLPA...
Descritores: Biópsia
Dinamina II
Exoma
Sequenciamento de Nucleotídeos em Larga Escala
Hipotonia Muscular
Miopatias Congênitas Estruturais
Canal de Liberação de Cálcio do Receptor de Rianodina
Limites: Seres Humanos
Masculino
Feminino
Lactente
Pré-Escolar
Criança
Adolescente
Adulto Jovem
Meia-Idade
Responsável: BR66.1 - Divisão de Biblioteca e Documentação


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Id: lil-732027
Autor: Rueda, Angélica; de Alba-Aguayo, David R.; Valdivia, Héctor H..
Título: Receptor de rianodina, fuga de calcio y arritmias / Ryanodine receptor, calcium leak and arrhythmias
Fonte: Arch. cardiol. Méx;84(3):191-201, jul.-sep. 2014. ilus.
Idioma: es.
Resumo: La participación del canal de Ca2+/receptor de rianodina en el acoplamiento excitación-contracción cardiaco se conoce desde finales de los años ochenta, cuando en varios trabajos trascendentales se comunicó por primera vez su purificación y se encontró que correspondía a las estructuras conocidas como «pies¼ localizadas en las cisternas terminales del retículo sarcoplásmico. Adicionalmente a su papel como canal responsable del aumento global y transitorio de Ca2+ que activa a la maquinaria contráctil durante el ciclo cardiaco, el receptor de rianodina también libera Ca2+ durante la fase de relajación, dando lugar a la fuga de Ca2+ en la diástole que en condiciones fisiológicas regula el nivel de Ca2+ luminal, pero cuando se encuentra alterada participa en la generación de arritmias adquiridas o hereditarias. Recientemente, el esfuerzo de diversos grupos de investigación se ha enfocado en el desarrollo de herramientas farmacológicas para controlar la fuga diastólica de Ca2+ que se presenta alterada en algunas enfermedades cardiacas. En esta revisión nos enfocamos en describir la participación del receptor de rianodina cardiaco en la fuga diastólica de Ca2+ así como los diversos enfoques terapéuticos que se han implementado para controlar su actividad exacerbada en la diástole.

The participation of the ionic Ca2+ release channel/ryanodine receptor in cardiac excitation-contraction coupling is well known since the late '80s, when various seminal papers communicated its purification for the first time and its identity with the "foot" structures located at the terminal cisternae of the sarcoplasmic reticulum. In addition to its main role as the Ca2+ channel responsible for the transient Ca2+ increase that activates the contractile machinery of the cardiomyocytes, the ryanodine receptor releases Ca2+ during the relaxation phase of the cardiac cycle, giving rise to a diastolic Ca2+ leak. In normal physiological conditions, diastolic Ca2+ leak regulates the proper level of luminal Ca2+, but in pathological conditions it participates in the generation of both, acquired and hereditary arrhythmias. Very recently, several groups have focused their efforts into the development of pharmacological tools to control the altered diastolic Ca2+ leak via ryanodine receptors. In this review, we focus our interest on describing the participation of cardiac ryanodine receptor in the diastolic Ca2+ leak under physiological or pathological conditions and also on the therapeutic approaches to control its undesired exacerbated activity during diastole.
Descritores: Arritmias Cardíacas/etiologia
Cálcio/fisiologia
Canal de Liberação de Cálcio do Receptor de Rianodina/fisiologia
-Diástole
Limites: Seres Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Revisão
Responsável: MX1.1 - CENIDSP - Centro de Información para Decisiones en Salud Pública


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Id: lil-723901
Autor: Carneiro-Júnior, M.A.; Quintão-Júnior, J.F.; Drummond, L.R.; Lavorato, V.N.; Drummond, F.R.; Amadeu, M.A.; Oliveira, E.M.; Felix, L.B.; Cruz, J.S.; Mill, J.G.; Natali, A.J.; Prímola-Gomes, T.N..
Título: Effect of exercise training on Ca2+ release units of left ventricular myocytes of spontaneously hypertensive rats
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;47(11):960-965, 11/2014. tab, graf.
Idioma: en.
Resumo: In cardiomyocytes, calcium (Ca2+) release units comprise clusters of intracellular Ca2+ release channels located on the sarcoplasmic reticulum, and hypertension is well established as a cause of defects in calcium release unit function. Our objective was to determine whether endurance exercise training could attenuate the deleterious effects of hypertension on calcium release unit components and Ca2+ sparks in left ventricular myocytes of spontaneously hypertensive rats. Male Wistar and spontaneously hypertensive rats (4 months of age) were divided into 4 groups: normotensive (NC) and hypertensive control (HC), and normotensive (NT) and hypertensive trained (HT) animals (7 rats per group). NC and HC rats were submitted to a low-intensity treadmill running protocol (5 days/week, 1 h/day, 0% grade, and 50-60% of maximal running speed) for 8 weeks. Gene expression of the ryanodine receptor type 2 (RyR2) and FK506 binding protein (FKBP12.6) increased (270%) and decreased (88%), respectively, in HC compared to NC rats. Endurance exercise training reversed these changes by reducing RyR2 (230%) and normalizing FKBP12.6 gene expression (112%). Hypertension also increased the frequency of Ca2+ sparks (HC=7.61±0.26 vs NC=4.79±0.19 per 100 µm/s) and decreased its amplitude (HC=0.260±0.08 vs NC=0.324±0.10 ΔF/F0), full width at half-maximum amplitude (HC=1.05±0.08 vs NC=1.26±0.01 µm), total duration (HC=11.51±0.12 vs NC=14.97±0.24 ms), time to peak (HC=4.84±0.06 vs NC=6.31±0.14 ms), and time constant of decay (HC=8.68±0.12 vs NC=10.21±0.22 ms). These changes were partially reversed in HT rats (frequency of Ca2+ sparks=6.26±0.19 µm/s, amplitude=0.282±0.10 ΔF/F0, full width at half-maximum amplitude=1.14±0.01 µm, total duration=13.34±0.17 ms, time to peak=5.43±0.08 ms, and time constant of decay=9.43±0.15 ms). Endurance exercise training attenuated the deleterious effects of hypertension on calcium release units of left ventricular myocytes.
Descritores: Cálcio/fisiologia
Ventrículos do Coração/metabolismo
Hipertensão/terapia
Atividade Motora/fisiologia
Miócitos Cardíacos/metabolismo
Condicionamento Físico Animal/métodos
-Sinalização do Cálcio/fisiologia
Teste de Esforço/métodos
Ventrículos do Coração/citologia
Hipertensão/metabolismo
Ratos Endogâmicos SHR
Ratos Wistar
Canal de Liberação de Cálcio do Receptor de Rianodina/genética
Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo
Proteínas de Ligação a Tacrolimo/genética
Proteínas de Ligação a Tacrolimo/metabolismo
Limites: Animais
Masculino
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-659013
Autor: Correia, Ana Carolina de Carvalho; Silva, Polyana Cristina Barros; Silva, Bagnólia Araújo da.
Título: Hipertermia maligna: aspectos moleculares e clínicos / Malignant hyperthermia: clinical and molecular aspects / Hipertermia maligna: aspectos moleculares y clínicos
Fonte: Rev. bras. anestesiol;62(6):828-837, nov.-dez. 2012. ilus, tab.
Idioma: pt.
Resumo: CONTEÚDO: A hipertermia maligna (HM) é uma doença farmacogenética potencialmente letal que acomete indivíduos geneticamente predispostos. Manifesta-se em indivíduos susceptíveis em resposta à exposição a anestésicos inalatórios, relaxantes musculares despolarizantes ou atividade física extrema em ambientes quentes. Durante a exposição a esses agentes desencadeadores, há um aumento rápido e sustentado da concentração de cálcio mioplasmático (Ca2+) induzido pela hiperativação dos receptores de rianodina (RYR1) do músculo esquelético, causando uma alteração profunda na homeostase de Ca2+, caracterizando um estado hipermetabólico. RYR1, canais de libertação de Ca2+ do retículo sarcoplasmático, é o principal local de susceptibilidade à HM. Várias mutações no gene que codifica a proteína RYR1 foram identificadas, mas outros genes podem estar envolvidos. Atualmente, o método padrão para o diagnóstico de sensibilidade à HM é o teste de contratura muscular para exposição ao halotano-cafeína (CHCT) e o único tratamento é o uso de dantroleno. No entanto, com os avanços no campo da genética molecular, um pleno entendimento da etiologia da doença pode ser fornecido, favorecendo o desenvolvimento de um diagnóstico preciso, menos invasivo, com o teste de ADN, e também proporcionar o desenvolvimento de novas estratégias terapêuticas para o tratamento da HM. Logo, esta breve revisão tem como objetivo integrar os aspectos clínicos e moleculares da HM, reunindo informações para uma melhor compreensão desta canalopatia.

CONTENT: Malignant hyperthermia (MH) is a potentially lethal pharmacogenetic disorder that affects genetically predisposed individuals. It manifests in susceptible individuals in response to exposure to Inhalant anesthetics, depolarizing muscle relaxants or extreme physical activity in hot environments. During exposure to these triggering agents, there is a rapid and sustained increase of myoplasmic calcium (Ca2+) concentration induced by hyperactivation of ryanodine receptor of skeletal muscle (RyR1), causing a profound change in Ca2+ homeostasis, featuring a hypermetabolic state. RyR1, Ca2+ release channels of sarcoplasmic reticulum, is the primary locus for MH susceptibility. Several mutations in the gene encoding the protein RyR1 have been identified; however, other genes may be involved. Actually, the standard method for diagnosing MH susceptibility is the muscle contracture test for exposure to halothane-caffeine (CHCT) and the only treatment is the use of dantrolene. However, with advances in molecular genetics, a full understanding of the disease etiology may be provided, favoring the development of an accurate diagnosis, less invasive, with DNA test, and also will provide the development of new therapeutic strategies for treatment of MH. Thus, this brief review aims to integrate molecular and clinical aspects of MH, gathering input for a better understanding of this channelopathy.

CONTENIDO: La hipertermia maligna (HM) es una enfermedad farmacogenética potencialmente letal que afecta a individuos genéticamente predispuestos. Se manifiesta en los individuos susceptibles en respuesta a la exposición a los anestésicos inhalatorios, relajantes musculares despolarizantes o actividad física extrema en ambientes calientes. Durante la exposición a esos agentes desencadenantes, existe un aumento rápido y constante de la concentración de calcio mioplasmático (Ca2+) inducido por la hiperactivación de los receptores de rianodina (RYR1) del músculo esquelético, causando una alteración profunda en la homeostasa de Ca2+, y caracterizando un estado hipermetabólico. RYR1, canales de liberación de Ca2+ del retículo sarcoplasmático, es la principal región de susceptibilidad a la HM. Varias mutaciones en el gen que codifica la proteína RYR1 han sido identificadas, pero otros genes pueden estar involucrados también. Actualmente, el método estándar para el diagnóstico de la sensibilidad a la HM es el test de contractura muscular para la exposición al halotano-cafeína (CHCT) y el único tratamiento es el uso de dantroleno. Sin embargo, con los avances en el campo de la genética molecular, un pleno entendimiento de la etiología de la enfermedad puede ser suministrado, favoreciendo así el desarrollo de un diagnóstico preciso, menos invasivo, con el test de ADN, y también proporcionar el desarrollo de nuevas estrategias terapéuticas para el tratamiento de la HM. Por eso, esta breve revisión intenta integrar los aspectos clínicos y moleculares de la HM, reuniendo informaciones para lograr una mejor comprensión de esa canalopatía.
Descritores: Hipertermia Maligna
-Hipertermia Maligna/diagnóstico
Hipertermia Maligna/genética
Hipertermia Maligna/terapia
Canal de Liberação de Cálcio do Receptor de Rianodina/fisiologia
Limites: Seres Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Sudo, R. T
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Id: lil-532288
Autor: Matos, A. R; Sambuughin, N; Rumjanek, F. D; Amoedo, N. D; Cunha, L. B. P; Zapata-Sudo, G; Sudo, R. T.
Título: Multigenerational Brazilian family with malignant hyperthermia and a novel mutation in the RYR1 gene
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;42(12):1218-1224, Dec. 2009. tab, ilus.
Idioma: en.
Resumo: Malignant hyperthermia (MH) is a pharmacogenetic disease triggered in susceptible individuals by the administration of volatile halogenated anesthetics and/or succinylcholine, leading to the development of a hypermetabolic crisis, which is caused by abnormal release of Ca2+ from the sarcoplasmic reticulum, through the Ca2+ release channel ryanodine receptor 1 (RyR1). Mutations in the RYR1 gene are associated with MH in the majority of susceptible families. Genetic screening of a 5-generation Brazilian family with a history of MH-related deaths and a previous MH diagnosis by the caffeine halothane contracture test (CHCT) in some individuals was performed using restriction and sequencing analysis. A novel missense mutation, Gly4935Ser, was found in an important functional and conserved locus of this gene, the transmembrane region of RyR1. In this family, 2 MH-susceptible individuals previously diagnosed with CHCT carry this novel mutation and another 24 not previously diagnosed members also carry it. However, this same mutation was not found in another MH-susceptible individual whose CHCT was positive to the test with caffeine but not to the test with halothane. None of the 5 MH normal individuals of the family, previously diagnosed by CHCT, carry this mutation, nor do 100 controls from control Brazilian and USA populations. The Gly4932Ser variant is a candidate mutation for MH, based on its co-segregation with disease phenotype, absence among controls and its location within the protein.
Descritores: Hipertermia Maligna/genética
Mutação de Sentido Incorreto/genética
Linhagem
Canal de Liberação de Cálcio do Receptor de Rianodina/genética
-Brasil
Contratura
Cafeína
Família
Testes Genéticos
Halotano
Hipertermia Maligna/diagnóstico
Limites: Feminino
Seres Humanos
Masculino
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-526098
Autor: Calderón-Vélez, Juan Camilo; Figueroa-Gordon, Lourdes Carolina.
Título: El acoplamiento excitación-contracción en el músculo esquelético: preguntas por responder a pesar de 50 años de estudio / Excitation-contraction coupling in skeletal muscle: questions remaining after 50 years of research
Fonte: Biomédica (Bogotá);29(1):140-160, mar. 2009. ilus.
Idioma: es.
Resumo: El mecanismo de acoplamiento excitación-contracción fue definido en el músculo esquelético como la secuencia de eventos que ocurre desde la generación del potencial de acción en la fibra muscular hasta que se inicia la generación de tensión. La regulación e interacción de dichos eventos entre sí ha sido estudiada durante los últimos 50 años utilizando diferentes técnicas, con las cuales se estableció la importancia y origen del ion calcio como activador contráctil, se conocen las principales proteínas involucradas y se inició el estudio de la base ultraestructural y de la regulación farmacológica; además, hay evidencias de que el acoplamiento excitación-contracción se altera en diferentes situaciones como en el envejecimiento, en la fatiga muscular y en algunas enfermedades musculares. Sin embargo, aún hay varias preguntas por responder: ¿cómo es el desarrollo y envejecimiento del mecanismo de acoplamiento excitación-contracción?, ¿cuál es su papel en la fatiga muscular y en algunas enfermedades musculares?, ¿cuál es la naturaleza de la interacción entre diferentes proteínas involucradas en el acoplamiento excitación-contracción? La presente revisión describe el acoplamiento excitación-contracción en el músculo esquelético y las técnicas utilizadas para su estudio como introducción para discutir algunas de las preguntas que aún falta por responder al respecto.

The excitation-contraction coupling mechanism was defined as the entire sequence of reactions linking excitation of plasma membrane to activation of contraction in skeletal muscle. By using different techniques, their regulation and interactions have been studied during the last 50 years, defining until now the importance and origin of the calcium ion as a contractile activator and the main proteins involved in the whole mechanism. Furthermore, the study of the ultrastructural basis and pharmacological regulation of the excitation-contraction coupling phenomenon has begun. The excitation-contraction coupling is thought to be altered in situations as ageing, muscle fatigue and some muscle diseases. However, many questions remain to be answered. For example, (1) How excitation-contraction coupling develops and ages? (2) What role does it play in muscle fatigue and other diseases? (3) What is the nature of the interaction between the proteins believed to be involved? The present review describes excitation-contraction coupling in skeletal muscle and techniques used to better understand it as an introduction for discussing unanswered questions regarding excitation-contraction coupling.
Descritores: Cálcio
Canais de Cálcio Tipo L
Contração Muscular
Fadiga Muscular
Relaxamento Muscular
Músculo Esquelético
Canal de Liberação de Cálcio do Receptor de Rianodina
Tipo de Publ: Revisão
Responsável: CO42.1 - Biblioteca Nacional de Salud José Celestino Mutis


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Id: lil-443671
Autor: Hidalgo, C; Bull, R; Marengo, J. J; Perez, C. F; Donoso, P.
Título: SH oxidation stimulates calcium release channels (ryanodine receptors) from excitable cells
Fonte: Biol. Res;33(2):113-124, 2000. graf.
Idioma: en.
Projeto: Fondo Nacional de Investigación Científica y Tecnológica.
Resumo: The effects of redox reagents on the activity of the intracellular calcium release channels (ryanodine receptors) of skeletal and cardiac muscle, or brain cortex neurons, was examined. In lipid bilayer experiments, oxidizing agents (2,2'-dithiodipyridine or thimerosal) modified the calcium dependence of all single channels studied. After controlled oxidation channels became active at sub microM calcium concentrations and were not inhibited by increasing the calcium concentration to 0.5 mM. Subsequent reduction reversed these effects. Channels purified from amphibian skeletal muscle exhibited the same behavior, indicating that the SH groups responsible for modifying the calcium dependence belong to the channel protein. Parallel experiments that measured calcium release through these channels in sarcoplasmic reticulum vesicles showed that following oxidation, the channels were no longer inhibited by sub mM concentrations of Mg2+. It is proposed that channel redox state controls the high affinity sites responsible for calcium activation as well as the low affinity sites involved in Mg2+ inhibition of channel activity. The possible physiological and pathological implications of these results are discussed.
Descritores: Canal de Liberação de Cálcio do Receptor de Rianodina/efeitos dos fármacos
Compostos de Sulfidrila/farmacologia
Córtex Cerebral/citologia
Miócitos Cardíacos/metabolismo
Neurônios/metabolismo
Retículo Sarcoplasmático/metabolismo
-Anuros
Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo
Oxirredução
Limites: Animais
Coelhos
Ratos
Responsável: BR1.1 - BIREME


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Cicogna, A. C
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Id: lil-439677
Autor: Vizotto, V. A; Carvalho, R. F; Sugizaki, M. M; Lima, A. P; Aragon, F. F; Padovani, C. R; Castro, A. V. B; Dal Pai-Silva, M; Nogueira, C. R; Cicogna, A. C.
Título: Down-regulation of the cardiac sarcoplasmic reticulum ryanodine channel in severely food-restricted rats
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;40(1):27-31, Jan. 2007. graf, tab.
Idioma: en.
Projeto: Fundação de Amparo à Pesquisa do Estado de São Paulo; . Conselho Nacional de Desenvolvimento Científico e Tecnológico; . Universidade Estadual Paulista. Faculty of Medicine.
Resumo: We have shown that myocardial dysfunction induced by food restriction is related to calcium handling. Although cardiac function is depressed in food-restricted animals, there is limited information about the molecular mechanisms that lead to this abnormality. The present study evaluated the effects of food restriction on calcium cycling, focusing on sarcoplasmic Ca2+-ATPase (SERCA2), phospholamban (PLB), and ryanodine channel (RYR2) mRNA expressions in rat myocardium. Male Wistar-Kyoto rats, 60 days old, were submitted to ad libitum feeding (control rats) or 50 percent diet restriction for 90 days. The levels of left ventricle SERCA2, PLB, and RYR2 were measured using semi-quantitative RT-PCR. Body and ventricular weights were reduced in 50 percent food-restricted animals. RYR2 mRNA was significantly decreased in the left ventricle of the food-restricted group (control = 5.92 ± 0.48 vs food-restricted group = 4.84 ± 0.33, P < 0.01). The levels of SERCA2 and PLB mRNA were similar between groups (control = 8.38 ± 0.44 vs food-restricted group = 7.96 ± 0.45, and control = 1.52 ± 0.06 vs food-restricted group = 1.53 ± 0.10, respectively). Down-regulation of RYR2 mRNA expressions suggests that chronic food restriction promotes abnormalities in sarcoplasmic reticulum Ca2+ release.
Descritores: Proteínas de Ligação ao Cálcio/metabolismo
Regulação para Baixo/fisiologia
Privação de Alimentos/fisiologia
Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/metabolismo
-Proteínas de Ligação ao Cálcio/genética
Regulação para Baixo/genética
Ratos Endogâmicos WKY
Reação em Cadeia da Polimerase Via Transcriptase Reversa
RNA Mensageiro/genética
Canal de Liberação de Cálcio do Receptor de Rianodina/genética
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/genética
Limites: Animais
Masculino
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-437527
Autor: Verkhratsky, Alexei.
Título: Endoplasmic reticulum calcium signaling in nerve cells
Fonte: Biol. Res;37(4):693-699, 2004.
Idioma: en.
Resumo: The endoplasmic reticulum (ER) is an important organelle involved in various types of signaling in nerve cells. The ER serves as a dynamic Ca2+ pool being thus involved in rapid signaling events associated with cell stimulation by either electrical (action potential) or chemical (neurotransmitters) signals. This function is supported by Ca2+ release channels (InsP3 and ryanodine receptors) and SERCA Ca2+ pumps residing in the endomembrane. In addition the ER provides a specific environment for the posttranslational protein processing and transport of various molecules towards their final destination. In parallel, the ER acts as a "calcium tunnel," which facilitates Ca2+ movements within the cell by avoiding cytoplasmic routes. Finally the ER appears as a source of numerous signals aimed at the nucleus and involved in long-lasting adaptive cellular responses. All these important functions are controlled by intra-ER free Ca2+ which integrates various signaling events and establishes a link between fast signaling, associated with ER Ca2+ release/uptake, and long-lasting adaptive responses relying primarily on the regulation of protein synthesis. Disruption of ER Ca2+ homeostasis triggers several forms of cellular stress response and is intimately involved in neurodegeneration and neuronal cell death.
Descritores: Retículo Endoplasmático
Canal de Liberação de Cálcio do Receptor de Rianodina
Sinalização do Cálcio
-Encefalopatias/etiologia
Neurônios
Limites: Animais
Responsável: CL1.1 - Biblioteca Central


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Id: lil-437524
Autor: Friel, David.
Título: Interplay between ER Ca2+ uptake and release fluxes in neurons and its impact on [Ca2+] dynamics
Fonte: Biol. Res;37(4):665-674, 2004. ilus, graf.
Idioma: en.
Resumo: In neurons, depolarizing stimuli open voltage-gated Ca2+ channels, leading to Ca2+ entry and a rise in the cytoplasmic free Ca2+ concentration ([Ca2+]i). While such [Ca2+]i elevations are initiated by Ca2+ entry, they are also influenced by Ca2+ transporting organelles such as mitochondria and the endoplasmic reticulum (ER). This review summarizes contributions from the ER to depolarization-evoked [Ca2+]i responses in sympathetic neurons. As in other neurons, ER Ca2+ uptake depends on SERCAs, while passive Ca2+ release depends on ryanodine receptors (RyRs). RyRs are Ca2+ permeable channels that open in response to increases in [Ca2+]i, thereby permitting [Ca2+]i elevations to trigger Ca2+ release through Ca2+-induced Ca2+ release (CICR). However, whether this leads to net Ca2+ release from the ER critically depends upon the relative rates of Ca2+ uptake and release. We found that when RyRs are sensitized with caffeine, small evoked [Ca2+]i elevations do trigger net Ca2+ release, but in the absence of caffeine, net Ca2+ uptake occurs, indicating that Ca2+ uptake is stronger than Ca2+ release under these conditions. Nevertheless, by increasing ER Ca2+ permeability, RyRs reduce the strength of Ca2+ buffering by the ER in a [Ca2+]I-dependent manner, providing a novel mechanism for [Ca2+]i response acceleration. Analysis of the underlying Ca2+ fluxes provides an explanation of this and two other modes of CICR that are revealed as [Ca2+]i elevations become progressively larger.
Descritores: Canal de Liberação de Cálcio do Receptor de Rianodina/fisiologia
Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo
Canais de Cálcio/metabolismo
Neurônios/fisiologia
Neurônios/metabolismo
Retículo Endoplasmático/fisiologia
-Citosol/fisiologia
Citosol/metabolismo
/fisiologia
INOSITOL 1,ABBREVIATIONS AS TOPIC,ABDOMEN-TRIFOSFATO/fisiologia
Limites: Animais
Tipo de Publ: Revisão
Responsável: CL1.1 - Biblioteca Central



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